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I recently came acroos this video : https://m.facebook.com/story.php?story_fbid=1053324651468913&id=492140647587319
I want to know whether these birds are real or edited? If they're real, what are their names?
Yes, they are real, that's not a CGI. That footage belongs to The Cornell Lab of Ornithology, and those are birds-of-paradise.
The first one is a Wilson's Bird of Paradise (Diphyllodes respublica). Here is an image of it:
The second one, showing a courtship display, is a Superb Bird of Paradise (Lophorina superba). Here is an image of it:
And the courtship display:
The third one is a King Bird of Paradise (Cicinnurus regius). Here is an image of it:
The next one is the Wahnes's parotia (Parotia wahnesi). Here is a picture of it:
The last one is a King of Saxony Bird of Paradise (Pteridophora alberti). Here is its picture:
Finally, here is the only correct way (just kidding) to watch any video with birds of paradise: narrated by David Attenborough! Have a look:
These Birds Can Sing Using Only Their Feathers
Imagine if you could make music with your ponytail or sing using just your beard. It sounds absurd, but some birds perform a feat not all that different. They make songs appear out of feathers and thin air.
The microscopic physics of how exactly feather sound works is a still bit of a mystery, says Richard Prum, an evolutionary ornithologist at Yale University, but scientists know that when air hits certain feathers—at the right speed and angle—it causes them to vibrate. And this rapid oscillation produces sound.
Prum and his colleagues described wing-singing, or aeroelastic flutter, in two species of broadbill, in a paper published last week in the Journal of Experimental Biology. The broadbills are small, mostly unremarkable birds native to East Africa. But the sound the birds make during their mating displays are difficult to ignore. The researchers compare it to the “aroogah!” of a mechanical horn and note that the noise can travel more than 100 yards through dense forest.
The broadbills’ mating flight sound requires what Prum calls a “stylized wing beat” with an “energetic down stroke.” In other words, when the birds flap their wings in everyday flight, it is mostly silent. The feathers only produce the characteristic “brreeeet” when the birds want to be heard.
Prum says broadbills are also unique in that no single feather seems to be crucial to the sound. Instead, different parts of six feathers vibrate in concert, and the birds can still produce sound even if one is taken away. (To figure that out, Prum and his colleagues brought a wing specimen back to the laboratory and manipulated it under various wind tunnel conditions.)
The idea that birds can make music with their wings may seem exotic, but it actually isn’t all that new. Charles Darwin even devoted a section to it in The Descent of Man back in 1871. What’s more, you don’t have to travel to some far-flung forest of Uganda to hear these sounds.
I heard my first wing-song last month in a small park outside of Pittsburgh, Pennsylvania. Dusk was just settling in, and while the rest of the wood was getting ready for bed, a small, long-beaked bird called the American woodcock was apparently feeling frisky.
Every February to April, male woodcocks perform what’s known as a “sky dance.” This involves a barrage of vocal “peents” from the ground before a burst of flight that unleashes whistling from the bird’s wings. For what seems like forever, the birds climb higher and higher into the sky, some 400 feet, before adding another, climactic vocalization and zig-zagging back to earth like a falling leaf—back to the very spot from which the performance began.
Woodcocks employ a combination of sounds made from both their voicebox, called a syrinx in birds, and their feathers. Think of it like the sound created by blowing on a blade of grass held between your thumbs, says Robert Mulvihill, an ornithologist at the National Aviary in Pittsburgh. “These birds are actually playing the instrument that is their wings.”
Mulvihill says aerial flights like the woodcock’s may be linked to reversed sexual dimorphism, a term for when males of a species are smaller than females. Smaller, swifter males may be better equipped to perform aerial acrobatics or create louder, more attractive sounds while doing so—and, thus, be better able to attract a mate.
If you know what you’re listening for, aeroelastic flutter is probably all around you—and this is probably true not just for people who stand in a meadow at dusk waiting for woodcocks. Hummingbirds, some of the most beloved backyard species across the United States, also make surprisingly loud chirps and tweets. And unlike the wing-singing of the woodcock and broadbills, hummingbirds make their music by shaking their tail feathers.
Christopher Clark, a colleague of Prum’s now at the University of California, Riverside, and lead author of the recent broadbill study, has made a career of studying hummingbird feathers and the sounds they generate. Each species emits a different frequency, usually by opening its tail feathers at the bottom of a blink-and-you’ll-miss-it courtship dive. These noises vary from a single, rapid “bleeeep” to fluttering notes that sound like a ray gun’s “pew pew pew.”
While hummingbird courtship can be cryptic, there’s nothing subtle about the common nighthawk. These birds, which are more nightjar than raptor, prey upon insects caught in midair and nest across most of the United States and Canada. While calling out to potential mates, these guys fly in high circles before rocketing out of the sky like a tractor-trailer barreling down a highway. The courtship dive culminates in a “boom!” as air causes the bird’s wing feathers to rapidly vibrate.
Some birds don’t even have to be in flight to play their feathered instruments. The male ruffed grouse just hops up on a log and starts thwapping away in rhythmic bursts that sound like the first few strokes of a gas-powered lawnmower. It’s common to hear this sound while walking in the woods from April to May pretty much anywhere from the Appalachians to Alaska, but actually seeing the bird perform its mating ritual is a rare treat.
While all of these feather sounds are related to courtship, Prum says there is one bird known to make a warning with its wing beats. The crested pigeon of Australia has modified flight feathers that create a distinctive flappety-whistle when it’s alarmed. What’s more, in a study published in 2009, researchers showed that when they played recordings of the pigeon’s wing sound, other pigeons hightailed it out of the area—a pretty clear sign that the sound is pigeon-speak for “run away!”
Credit to Robert Magrath, Australian National University
Whether it’s wings or tails, one modified feather or a bunch of completely normal looking ones, super-quick flights or while sitting still on a log, Mulvihill says birds have come up with just about every way to make noise.
List of Colorful Birds
Here we go! Welcome to the world of colorful birds!
1. Red-necked Tanager
Endemic to Eastern South America, the red necked tanager appears to be very bright with its yellow-orange wings, bright red chin, deep blue crown and lower neck, and a brilliant green underneath.
- These colourful birds are known to reside in the canopy of forests and are characterized by their sharp “sip” sounding voices.
- Generally, the red-necked Tanager molts (sheds its feathers) once in a year.
2. Mandarin Duck
Regarded as the world’s most beautiful duck, this native from China (hence the name) and Japan, this duck displays a wide array of colors such as blue, green, copper and silver.
- While both genders of the duck have crest, this structure is more prominent on males, probably because this is mainly used to attract during mating.
- In addition to that, males appear to be golden in appearance.
3. Blue Crowned Pigeon
Also known as the Western crowned pigeon, the blue crowned pigeon is characterized by having large blue crests in the head, and deep blue feathers around the eyes.
- Western crowned pigeons are very large pigeons and in fact considered as one of the “fairest” members of the Family Columbidae (Pigeons).
- Generally, like most birds in the animal kingdom, male blue crowned pigeons are larger as compared to their female counterparts.
- These colorful birds are native to Papua New Guinea and they tend to be dispersed in the rains-forests of the islands.
4. Blue/Azure Kingfisher
Known to be great fish hunters from the riverside and sometimes above the water surface, blue kingfishers are small to medium size birds which have very colorful appearance.
- The feathers of kingfishers are mostly bright blue/azure (hence the name) in color.
- Unlike most birds, the feather color of kingfishers is caused by the structure of the feathers themselves. Such causes the scattering of blue light and is then reflected in our eyes, making them appear blue.
- The distribution pattern of kingfishers is cosmopolitan. Meaning, they occur throughout the world, even in either temperate or tropical regions.
5. Paradise Tanager
Classy, neotropical, and colorful, the Paradise Tanager is really living up to its name. This bird, widely distributed in the tropical forests of the Amazon in South America, is small yet very colorful with its bright apple green head, yellow or red rump (depending on species), and a blue abdomen.
- Aside from its appearance, the paradise tanager is a songbird, meaning, it can make various musical sounds that are pleasant to the ears.
- One disclaimer though, this bird is not found in Chile, despite its species name T. chilensis.
6. Andean Cock-of-the-Rock
Considered the national bird of Peru, this small to medium sized bird made it to the list of most colorful birds.
- Male Andean Cock-of-the-Rock birds are more colorful with their bright red head, breast, throat, and shoulders. They have grey wings, an overall black underparts, and a very prominent disk crests over their bill.
- On the other hand, the female birds are orange to brown in color and have smaller crests.
- This bird is usually found in the warm regions and usually reside riverbanks and forest streams.
7. Purple Gallinule
The Purple Gallinule is considered as one of the most beautiful birds primarily because of its plumage that displays a variety of colors.
- Overall, this bird has a purple head, throat, and underparts, a green back,a blue forehead, and a red beak with yellow tip.
- Added to this uniqueness is its legs which are yellow in color.
- Interestingly, these colorful birds swim like ducks but can step on floating leaves like chickens.
- Basically, this species of bird is widely distributed in the humid and tropical regions of the United States.
8. Yellow-collared Lovebird
Also known as Masked lovebirds, yellow collared lovebirds are small colorful birds which are generally green in appearance (although upper parts are darker). In addition to that, they have black-colored heads and white eyerings, and very bright red beaks.
- As their name suggests, they have yellow collar which is extended to the nape of the neck.
- Interestingly enough, the males and females of this species look identical in appearance.
- These colourful birds are endemic to Tanzania but were already brought to other countries like Kenya and Burundi.
9. Northern Cardinal
Endemic to both North and South America, the Northern Cardinalis bird is a songbird characterized by striking red and black face mask which extends up to the upper chest.
How does evolution work?
Evolution is simply the change in the gene pool of a population over time. Individual organisms don’t evolve once you have your genes, they can’t really be changed except for a very few rare circumstances. But there are five different ways that genes can change a population over time:
Mutation is very important in evolution because it’s the only way that completely new genes ever happen. In fact, every single gene in the world started as a mutation! The other four mechanisms are just different ways that genes can be reshuffled, but with mutation, it’s something new that’s never been seen before.
Most mutations don’t have any effect on the organism, or they may even have a negative effect. But, every once in a while, a mutation happens that actually improves the organism in some way. Maybe it’s just a bit faster, has sharper teeth, or a better brain. When this happens, the organism is more likely to survive, reproduce, and pass on the new gene to its offspring. When those genes spread in the population, it’s said to have evolved.
When organisms move in and out of an area, they also take their genes with them!
In conservation, one of the main concerns is how the wild landscape is becoming increasingly fragmented. More roads, farms, and shopping malls are built, and shy animals don’t move around like they did historically.
Now, a very real possibility is that some populations will become too isolated and may eventually evolve to become inbred. If this happens, they’re more likely to succumb to disease or be unable to adapt to a changing environment because they won’t have access to new genes that may help them survive better.
It might seem like “natural selection” is a difficult-to-understand concept dating back to Darwin and his Galapagos finches, but it’s actually pretty simple.
Organisms are exposed to different conditions that affect how likely they are to survive and have babies. That’s it! These different conditions, called selective pressures, can be external (in the environment) or internal (within their own bodies).
Examples of selective pressures might be the pH of ocean water (crab shells will dissolve when it’s too acidic), a new disease (Tasmanian devils are evolving to become more resistant to an infectious facial tumor), or how attractive an organism is to others (“beautiful” or “handsome” animals are more likely to find mates and reproduce than their “ugly” counterparts).
Artificial selection is similar to natural selection, except the limitation to which organisms are allowed to reproduce is decided by humans. We do this because we want to develop a certain trait in an organism, like high-productivity wheat or friendlier kitties.
Check out this cool example of artificial selection in some things you may eat all the time:
Dogs are a great example of artificial selection. There are 340 different breeds of dog in the world, all created by people for a certain purpose. In some cases, such as English Bulldogs or Chihuahuas, these dogs’ genes are manipulated to make them physically attractive but can actually cause unhealthy side effects. It’s not very likely that these dogs would have evolved as such in the wild.
Most genes don’t have selective pressures on them forcing them to evolve one way or another. They just casually float along in a population, and each time a new organism is born, its genes from its parents get reshuffled randomly.
This has some interesting effects. If a population is very small, it’s more likely to show a phenomenon called genetic drift—random changes in the gene pool. Larger populations serve as big reservoirs of rare genes so it’s hard to lose them completely. On the flip side, it’s easier for rare genes to be lost from small populations because there aren’t very many to begin with.
For example, let’s think of a small population of just 20 birds. If only one of these birds has a rare gene and that bird dies, that gene is lost from the population. But, if there are 10,000 birds and 50 of those birds have the rare gene, that gene is much more likely to stay in the population by passing it on to offspring. It’s unlikely that all 50 of the special birds would be struck by lightning at the same time!
What lives in caves? Cave biodiversity
Caves are home to a variety of organisms, both those that live in the caves part of the time, or those that live in caves for their whole lives and never see the outside world. Due to the lack of light, there is normally an absence of plants, except for those that grow around entrances or openings in the cave roof that allow for sunlight to enter. Otherwise, sometimes seeds drift in and grow a short but then die quickly.
Due to the lack of primary production, most nutrients in a cave need to come from outside. Animals that use caves mainly for shelter while sleeping are a big part of the nutrient input for these ecosystems they do this by feeding outside and then coming inside to rest, bringing nutrients with them, mainly in the form of feces. Many animals in caves survive off of the excrement of these animals, such as guano from bats (which is just a fancy name for bat poop really). As well, some nutrients are brought in from being washed in by water from above or through flowing rivers.
The most obvious example of an animal that uses caves for part of the time are the many species of bats, which use caves to sleep in during the day but go outside at night to feed. As well, there are some nocturnal birds that use caves just like bats, such as the famous Oilbirds (S teatornis caripensis ), or Tayo or Guácharo in Spanish. These birds are also nocturnal, sleeping in caves during the day and coming out to feed at night. They have similar echolocation abilities and can fly in short erratic movements, much like bats. Larger animals may also use caves as temporary shelters or even dens to raise their young, but they do not tend to go too far past the entrance either. As well, various invertebrates that can manage well in the dark (because they rely little on their sight), like tarantulas or scorpions, may be found venturing into caves looking for food, though they aren’t necessarily true full time cave dwellers.
So what about things that live in caves all the time? Animals adapted to cave life, that never leave the cave, are referred to as troglobites . These animals include mainly insects, arachnids, and fish that are adapted to life in caves and actually never see the surface. Some examples are collembolans (springtails), cave crickets (Family Rhaphidophoridae), pseudoscorpions (Pseudoscorpionida), tailless whip scorpions (family Phrynidae), and a few interesting fish such as the Mexican tetra ( Astyanax mexicanus ) or the Andean Astroblepus photeter .
Interestingly, caves tend to be low in biodiversity because it is such a harsh environment, but they add a lot to biodiversity as a whole because species from cave to cave are often very different. Why? Well, the isolation between populations of organisms in different caves creates a phenomenon called allopatric speciation , which is when one population of animals is geographically isolated from another and they become different species over time because they can not reproduce with one another, causing them to become genetically distinct.
When asked to write the unabridged history of this organization, I was taken aback. I knew that I had reached many thousands in my quest to spread the truth, but I was bewildered and frustrated with myself when I realized that I had not yet done an acute job of giving details: the why, the how, when, who, etc. I knew that I had to write something that was concise, accurate, and free of any fault or error.
Prepare to take a journey into a history that they will not, dare I say- never teach in school. Much of what you are about to read has been censored for almost 60 years who knows how long it will take our corrupt government to block this website? Only time will tell. In the meantime, I ask that you take 20 minutes out of your busy day and read all of this information, soak it in… revel in the fact that everything you know
In 1947 the C.I.A. was founded, its sole responsibility to watch and survey tens of thousands of Americans suspected of doing communist things. This orchestrated stalking epidemic went on for almost 5 years, and few were found guilty of any real crimes. However, it became clear in the early 1950s that the threat of communism was only going to rise, and a broader system was needed to track any individual who was suspected of such activity. The fears were only encouraged when in 1951, Julius and Ethel Rosenberg were wrongly arrested and convicted of espionage against the United States- accused of spying on behalf of the Soviet Union (the big boy communist people.) This highly publicized event gave the government a small window to implement a new program that would place the first CCTV surveillance cameras in areas with a high Russian immigrant concentration.
This went on for a few years or so, when in 1953 Allen Dulles was made the first civilian director of the Central Intelligence Agency (C.I.A.) and made it his mission to ramp up the surveillance program hiding cameras in thousands of locations and ordering his staff to plant them in areas that would be impossible to detect (although let’s face it, in the 1950s- you could walk into a bank with a slingshot and steal thousands of dollars. Security was one big joke.) He knew that the possibilities for this camera program were endless, and on April 15 th , 1956 met with President Dwight D. Eisenhower and proposed a plan that would putcameras in the sky. Dulles knew that the sky was the future for his surveillance program, as you could truly track someone with a moving camera- much easier than having to switch between cameras on street corners and hidden in storm drains. One camera in the sky could do the work of hundreds on the ground…
Eisenhower approved the initial idea and asked him to return when he had figured out how to make it possible. Dulles left the oval office and immediately flew to an undisclosed location- meeting with various members of his inner circle, to discuss the plan in more intricate detail. It is believed that the initial plan for killing all of the birds and replacing them with flying cameras was thought up one weekend in May of 1956. Dulles and his team hated birds with a passion, and were heard on many occasions calling them,” flying slugs” and,” the scum of the skies,” as they would often poop on their cars in the parking lot of the C.I.A. headquarters, and quite frankly- all over the D.C. Metro area. I believe this was one of the driving forces that led Dulles to not only implement robots into the sky, but actually replace birds in the process. They did not need to kill all of the birds, and could have launched a quarter of the robot birds that they did, but the pigeons in D.C. at the time were absolutely ruthless… they were eating very well, as American moral was high- people were feeding them much more in public parks and on the street. This in turn created huge amounts of pigeon feces, that would inevitably find its way to the windshield of many men and women- all of whom grew to not only hate pigeons, but all birds. In a stolen transcript from an ex-CIA deputy, she says,” yeah, the higher ups were so annoyed that birds had been dropping fecal matter on their car windows that they vowed to wipe out every single flying feathered creature in North America.”
In this meeting they sought to kill two birds with one stone and remove all birds from the United States (thus eliminating their fecal problem), but also replacing these birds with billions of sophisticated robot look a likes- capable of mimicking real birds in every way. Dulles and his team wanted to create the greatest surveillance system ever imagined, with the capability of tracking someone on foot, in a vehicle, or even in their personal home.
It is imperative that we discuss the methods that the government used to extinguish over 12 billion birds between 1959 and 1971. If we are to make disciples of the birds aren’t real movement, we must equip each and every person with the knowledge of what truly happened in this saga of insanity and government corruption. Here are the facts and eyewitness accounts of various key events that occurred within our nation that completely destroyed every man woman and child bird in existence.
I touched on him for a brief moment in the last chapter, but I want to dive in to Allen Welsh Dulles: the Director of the Central Intelligence Agency from 1953 to 1961. Upon the government writing the plan to slowly kill off the birds, it was his responsibility to make it a reality. He was given the task of reallocating 65 Billion dollars of public health funds towards the forced extinction. On May 6 th , 1957 he met with an unidentified man from the Boeing Airplane Company and ordered 120 B-52 bombers. Dulles knew that if his government was to go undetected, he had to keep these aircraft out of sight from the American public. He was under strict orders not to leave a trace of his actions, so he devised a plan to construct the aircraft in Nevada’s Area 51. This way, the citizens of Seattle Washington (where Boeing was headquartered) wouldn’t be able to claim that the bombers had been built nearby (if the government was exposed).
23 men from within the Boeing Engineering department travelled to Area 51 in the back of an old school bus that they purchased from a salvage yard in Mukilteo Washington. They were seen by a few individuals bringing couches and rugs into the bus, and were also heard discussing and I quote,” really cool playlists for the road trip.”
Clearly, the Boeing Engineers didn’t get the memo from Dulles about remaining undetected, and actually painted “Area 51 or bust” on both sides of the bus. Whenever they would stop for gas, they would set up a makeshift campsite in the parking lot and sing songs with titles such as “I left my Honey for Area 51,” and,” Let’s Kill all the Birds.” They attracted a lot of attention, and the locals of a town in Idaho claimed that the men would reveal intimate details of what they were doing. Clearly, they were complete idiots but their idiocy is one of the hardest pieces of evidence on how the government killed the birds. While 22 of the men made it to Nevada, one man did not. Neil Ford was the only engineer that lived to tell the story, as he was left in a Waffle House bathroom because the others claimed,” he had to pee too many times, and was ruining the vibe of the road trip.”
Neil spoke with one of the founding members of the Birds Aren’t Real movement shortly before his death in 1994. He spoke about the way in which Dulles searched for the engineers who didn’t have families. That way, they would be able to disappear from the map when the project was complete, and nobody would notice. This disturbing reality is a far cry from the way in which many people view the 1950s and proves that our government has been ruthless in its effort to rid our nation of its peace and prosperity.
Upon making it to Area 51, the 22 remaining engineers were tasked with designing a new version of the B-52, the B-52B. The B stands for Bird or Barack, and it was to be a brand-new model of the B-52 that had 450-gallon water tanks in the place of the bomb compartments. The water tanks were hard to design, and one of the engineers almost gave up, but Dulles hit him over the head with a 40-pound wrench to try and “knock some sense into him.” This unintentionally put the man into a coma, to which he never awoke. Scared out of their minds, the remaining 21 engineers vowed to finish designing the airplane so they could leave Area 51 for good. This was to be a faulty dream however, as none of the men were ever seen again. We only know this information because 12 pallets of classified documents were stolen from a warehouse by one of our Birds Aren’t Real patriots- but we’ll get to that later.
Once the water tanks were fitted into each bomber, a complex system of radar and tracking technology was installed to the nose of the aircraft. This technology was extremely advanced for its time and was used by the crew to track large flocks of birds from distances of 200 miles away. Once the radar was fitted, 5 coats of jet-black matte paint was sprayed onto every surface of the plane. This was done to camouflage the aircraft against the night sky, so that it could go undetected from the ground. Not only was paint used to hide the bombers, but each external strobe, beacon, and landing light was removed. Not a single light emitted from the plane, and the Pratt & Whitney JT3D engines were fitted with noise reduction pads that enabled the aircraft to fly completely silent from altitudes of 3,000 ft. or higher.
It took 2 years to build the 120 bombers, and once they were finished, the Boeing Engineers were told that they were free to go home. However, they were intercepted 30 minutes into their trip back to Washington and were put in the back of an armored troop transport vehicle. The men were sent to the front line in Vietnam, which Dulles hoped would seal their fate. Each of the engineers actually survived for 3 weeks in intense combat and were kidnapped by the Viet Cong only after they ran out of ammunition. The men were not heard from again.
Now you may be wondering, how were the birds actually killed? What method was used to accomplish this act of mass murder? Good question. The water tanks in the bombers were filled with a specially formulated bird poison, that once consumed, would give the bird a virus that could be passed onto other birds. The poison was sprayed from an altitude of 8,000 feet and would completely dissolve before it hit the ground. Which meant that only birds would be affected by its terror, and once a single drop of the poison struck the birds feathers, the virus would take hold through the fibers and make its way into the bloodstream. The virus would then affect the bone structure in such a way that total decomposition of the birds would take place within 24 hours.
On June 2 nd , 1959 operation “Water the Country” was born. This was to be the secret code name given to the program from 1959 to 1976, when it was renamed to “Operation Very Large Bird” (the individual in charge of naming the program didn’t want to get into any copyright trouble with the popular PBS show Sesame Street by naming the project Operation Big Bird.) Within the next 6 years, 15% of the bird population was wiped out. During these first few years, bird prototypes were released by the hundred million. The term ‘drone’ was not used at this time, and instead they were referred to as Robot Birds.
Let it be known, the CIA were originally the only ones responsible for this atrocity, and the sitting President (John F. Kennedy at this time) had no idea that this was taking place. The CIA did not intend for anyone but select departments to find out what was going on, even the pilots of the bombers were unaware what they were doing. The Chief Commanding Officer of Water the Country told them that they were,” watering the grass of the entire country” To this day, it is highly unlikely that the pilots know that they assisted in the largest mass murder in world history. If any of the original bomber pilots of operation Water the Country are reading this, here me closely. We do not blame you for the sins of your superiors. While you did kill billions of helpless birds, you did not know what you were doing. You do not have to remain in hiding, join the movement and together we can fight the government.
As I said a few paragraphs ago, the President was unaware what was going on until October 3 rd , 1963 when a top CIA official was overheard speaking about the operation over a tapped phone. John F. Kennedy was the President at this time and had tapped the phone of Alvin B. Cleaver (Internal Communications Director for the CIA). Kennedy believed that Cleaver was stealing his ham sandwich from the White House Kitchen and vowed to catch him speaking about it over the phone. Instead, he heard a highly sensitive conversation that Cleaver was having with Dulles. In it, Cleaver said,” yeah Allen. I’ve stolen John’s lunch again haha, he doesn’t even know. I’m going to keep stealing it until he launches a full investigation. Then I’m going to plant a hidden camera and catch his reaction as I dump all the stolen sandwiches on his desk at one time. I’m going to call the new show ‘You’ve Been Cleavered.”
Dulles responded, “Haha Alvin, that’s going to be so funny. We’ll have to play that clip at the White House Correspondents dinner. By the way, how’s the bird slaughter going? How many birds have we killed so far?”
“We’ve killed about 220 million so far, and the best thing is, the Robot Birds we’ve released in their place have done such a good job that nobody even suspects a thing.”
Kennedy heard this conversation over the tapped phone and immediately called both into the Oval Office he demanded to know what they were discussing. They confessed what was taking place in the American sky late at night and he was appalled. He told them to stop the operation at once or he would fire them. They both explained to Kennedy why the birds needed to be exterminated and asked him if they could show Kennedy a prototype of one of their birds before he made any decisions on whether to end Operation Water the Country.
On October 25 th , 1963 Kennedy was shown a prototype of the Turkey X500- a robot that specialized in killing larger birds like eagles and falcons. The robot displayed its surveillance skills, as well as its ability to find and track escaped criminals (as we learned from chapter 1, this was one of the things that drove Eisenhower to approve the project.) Kennedy was impressed with what he was shown but continued to demand the immediate shutdown of the operation and less than a month later he was dead. Now I’m not saying that these events are correlated, but I am. JFK was murdered by the CIA because he was against the mass murder of every feathered flying creature in the United States. He was to be the first and only President to stand against the murder of the birds from Lyndon Johnson to Donald Trump, every President we’ve had since has turned a blind eye to the atrocities that began in 1959. After Kennedy was killed, the CIA started rigging elections. They would only allow candidates who were anti-bird and pro citizen surveillance to win the Presidency.
By now you must be shaking with fear. The thought of your government doing these things is too much for you to handle, can it really be true? Could the government have killed billions of birds and replaced them with robots? Yes, they did, but don’t feel alone. At any point during the reading of this book, you are free to email our counseling department ([email protected]) and we will walk you through the steps to mentally overcome this nightmare. I personally had to deal with this reality on my own, decades ago. Now I’m giving you a service that I wish had been available to me at the time of my discovery. If you’re currently experiencing episodes of excessive perspiration and muscle spasms because of what you’ve read, do not read Chapter 3 yet. If the first few chapters shocked you, chapter 3 will bring you to your knees. Buckle up, the nightmare is just beginning.
Chapter 3: The Winner Writes the History Book
On July 2nd, 1964 there was a secret meeting held in the Jefferson Building (Washington D.C.) The attendees are unknown, as the only evidence is a 6-minute recording that was uncovered in the basement of an isolated storage warehouse by one of our Patriots. In this meeting, it is believed that members of the C.I.A. and operation Water the Country (W.T.C. for short) discussed the need for a heavy amount of Bauxite, an amorphous clayey rock that is the chief commercial ore of aluminum. This bauxite was essential to the process of robot construction, as aluminum would make up roughly every facet of its frame and internal structure. In the audio recording from the meeting you can clearly hear one of the attendees say,” we need a quick solution to this problem, the production team needs this material right now. Real birds have been disappearing for almost 2 years now, and if we don’t start replacing them in mass quantities, people will notice. We need a solution in 30 days.”
This is where the recording stops.
Please buckle up for this next part. I don’t mean an America’s Car Mart used 1998 Honda Civic seat belt I mean a fighter jet ejection seat harness. Almost a month after this secret meeting, a North Vietnamese Torpedo boat was accused of attacking a U.S. Destroyer in the Gulf of Tonkin. It is widely believed that this incident was faked- and I concur. This incident was an excuse for the United States to place a huge number of troops in Vietnam and engage with the North Vietnamese on a much more escalated platform.
The question is, why would the U.S. want to fake such an incident? What would they have to gain from invading Vietnam? Surely nobody still believes the ‘to stop communism’ lie that was so fervently spread? Well you are in luck, because for the first time in history- you will finally know the truth. You will finally know why the United States of America decided to waltz into a small country on the tip of East Asia.
The nation of Vietnam contains the third largest reserves of Bauxite ore on the entire planet. Like I said earlier, this ore was the primary component of aluminum- which would be used to create the robots. The U.S. used the already brewing conflict in Vietnam to their advantage, and from 1964 to 1975, the U.S. attempted to invade and extract as much of this ore as possible, because without it- there would be no robot birds.
The process looked like this: U.S. soldiers were told to advance into an area of North Vietnam where they could “fight communism the best” (this is what they were told.) They were actually capturing areas that had enormous quantities of bauxite ore. Once flanking defenses were set up, dozens of excavators were deployed to dig into the deposit and dump the bauxite into dump trucks, that would then travel a distance of up to 26 hours through enemy territory- to Cam Ranh Base, a U.S. military port located in theKhánh Hòa Province of South Vietnam. The bauxite ore was then loaded onto a cargo ship that would deliver the ore to an unidentified port on the East Coast of the United States. From there, the ore would be transported to the hundreds of facilities that constructed the robot birds.
These facilities are believed to be located within many of the government fallout shelters and ammunition bunkers (one of the more modern factories is located underneath the Denver International Airport.) You see, the government escalated the fears of a Nuclear War during this time period (1960s-1980s) as an excuse to build massive underground warehouses, under the disguise of being “bomb shelters.” These facilities were so massive that hundreds of workers could fit inside and construct up to 5,000 robot birds per day. There are believed to be 22 of these underground manufacturing plants and during the peak of the construction process (sometime around 1980)- upwards of 100,000 robots were being constructed each day, across all 22 bunkers. However, each of these fake fallout shelter/ robot bird construction facilities would construct a different type of bird, specific to that region. For example, in Colorado- there is a bunker near Colorado Springs that specifically builds hummingbirds, as they used to be the primary backyard bird in the state (fun fact: hummingbirds are the ideal candidate for surveillance in a tight space, as they are small yet versatile.)
Now you may be wondering,” how did the government get thousands of people to build the birds, and where are they now? Why aren’t they testifying in court to the atrocities they were forced to commit, do they not remember building all those robot birds?” My friend, that question has been debated for decades by many within the Birds Aren’t Real community.
To sum it up, they were tripping balls.
The government would send individuals to local night clubs and bars- who would then scope out a candidate who looked like they could assemble a robot bird, and would tell that person that they were having a costume party on acid. It was the 60s and 70s, where acid was more accepted than bottled water. These people were then given work overalls (their costume) and a small tab of “acid” which was actually just a piece of colored paper. The ‘acid trip’ they expected was actually the bus ride to the entrance of the bunker, where they were given a tool box and a pair of headphones that played Pink Floyd nonstop. This combination of assembling a robot bird inside a 5 story government fallout bunker led them to believe they were on the most insane trip of their life.
Many of these individuals would later be heard saying,” the craziest trip I had was back in ’76 when I met this guy who gave me this crazy tab- from then all I remember is riding through the desert for 45 minutes on the top of a sawed off school bus, then walking down a stair case into a huge warehouse that was underground, and having some guy tell me to follow some instructions and make some sort of flying robot bird.”
There you have it, the reason why so many contributed to the construction and why none of them remember.
One of the main questions we have received lately goes as follows,” hello, when did the movement begin?” Well patriot, this chapter will address that very question. It all started in 1973, a time when the Vietnam War was ending, and thousands of U.S. troops were returning home. Operation Water the Country was handed over to William Colby, the new head of the C.I.A under President Gerald Ford. Colby renamed Operation Water the Country to Operation Very Large Bird and enacted an internal rule that anyone who had worked on the original Operation Water the Country was to be released of their duties and removed from their position. It had been over 10 years since the operation had begun, and they had only managed to replace 26% of the bird population with robots. This was 35% under target, and Colby wanted to hire men and women who would get the job done faster.
This proved to be a huge mistake.
One of the men Colby fired turned out to be the first whistleblower and risked his life to share the information that you’ve been reading, his brave actions started this entire movement.
It was a cold, rainy night in November 1973, the man (who shall remain nameless as we do not know his name) showed up on the doorstep of Clark Griffin, a young teenager from San Francisco. Clark had been an outspoken activist during the tail end of the Vietnam War, and now that the war had ended (all of the Bauxite was extracted, we now know) the Master knew that Clark would need another cause to campaign. As the soft raindrops pattered on the sidewalk below, the man (who shall be referred to as ‘the Master’) knocked on the door of Mr. Griffin’s apartment- you see, the Master knew that Colby most likely had people hired to follow him, as he knew information that could take this country down- so he couldn’t be seen meeting with any members of the newspaper, or television. The Master knew that he had to share what he knew with someone young, someone bright, who could be the face of the resistance. He knew that if he tried to start the movement himself, he would never be seen again.
Clark was an outspoken activist against the Vietnam War, and now that the war had ended- the Master wanted to give him something new to campaign against- the government atrocities of the 60s and 70s surrounding the bird genocide. The Master relayed everything he knew to Clark, and secretly helped launch the first Birds Aren’t Real movement…
Griffin was absolutely shocked to learn what the Master knew- but was not surprised. He was used to fighting the all-powerful United States government, and wanted to share his new found knowledge as fast as he could… He quickly formed a team from the original members of his Pro Peace/ Anti War campaign and tasked them with travelling to various college campuses across the United States and standing on street corners and in amphitheaters in these said campuses- preaching the feathered gospel and awakening many students- quickly forming a huge activist base.
This quickly became known as “The Tour of Freedom” by Clark and his team, as they would travel from university to university in the span of a few months at a time… teaching and informing anyone who dared listen to them. When they weren’t touring, they were researching and calling politicians, trying to find at least one individual who would grant them an interview…
It only took a few months for the team to realize that their supporters had grown so large that they needed to hold a public rally to show the government just who they were dealing with, and what they were up against. They needed to show the government that they weren’t about to go down without a fight… so Clark and his team organized a rally in the nation’s capital: Washington D.C.
This rally was attended by upwards of 2,000 people, mainly supporters from various college campuses who had driven through the night just to protest and show their support, true patriots(a phrase we do not take lightly.) During the rally the secret service was ordered to confiscate any film being taken of the event, to prevent it from being aired on television. This is a shame as we now do not have any images of this historic event, but only have the words of those who attended. These rallies would be held every year following 1974 until 1993- when the government officially put an end to the first Birds Aren’t Real movement.
Clark and his team continued to campaign and build support, calling politicians (to no avail) and travelling to public forums to voice their truth. They reached a tipping point in 1987 when they attempted to release an advertisement on national television during Super Bowl 21 however, the government stepped in and confiscated the original film, banning the ad under fears of ‘compromised national security.’ Quickly after this event, the offices of the Birds Aren’t Real movement were raided by the FBI and many of the important documents given to Clark- by the Master- were confiscated and placed in a top-secret location. The team did not let this affect them, and continued to try as hard they could to spread awareness and bring the heinous crimes to light- holding rallies until 1991 when Clark Griffin disappeared during the ’91 rally in San Francisco, last seen holding a sign and marching up Market St.
Nobody has seen or heard from him since that day, a day many of us in the movement call- Blue Monday (May 6 th .) Sadly, we do not have much information on what happened between the ’91 rally and 2017, a massive amount of time that we could’ve accomplished so much for the movement… but we cannot let that get us down. We must push full steam ahead and regain all the lost ground, in an effort to take back America from those that seek to destroy it.
If you’ve made it this far, I thank you. I thank you for your dedication to learn the truth and seek justice for the innocent birds that were taken from us. I have one more subject to discuss, a parting gift if you will- the current state of the movement. As of this writing- it is August 2019. Donald Trump has used sophisticated tactics to keep our movement suppressed, he knows that he can’t regulate the internet as well as he would like to. Google, Facebook and Instagram are independent platforms, being used by the government to track and compile data from the billions of drone birds cruising the skies all across America. Instagram has begun the process of censoring our message, as they remove post after post. Other movements have sprung up all across the world, as millions of people fear that their government is also not to be trusted. While there is zero evidence to suggest that countries in Europe have enacted this process of removing birds in replace of robots, the fear is still alive and well- for good reason.
A common question that we get a lot is, how do the birds not fly out of the United States to Mexico and Canada? Great question. While the majority of the birds are programmed to not cross over into these countries, there are some that still venture into these countries for a few reasons: picking up drugs (cocaine, marijuana, etc.) for eventual delivery into the lower-class segments of our major cities. The government will do anything they can to maintain control over its citizens, even getting them hooked on drugs. Another reason is simple- keeping tabs on U.S. citizens who go on vacation. Any bird you see flying across the U.S. borders to either Mexico or Canada is simply tracking an American citizen who has travelled outside the United States. However, there is currently nothing keeping a bird from Canada or Mexico from travelling inside America, which is why there will never be a 100% robot bird population, it will most likely hover around 95%- as birds are always flying in from our neighboring countries.
This may change soon, however. In 2016 President Trump announced that if he was elected, he will ‘build a wall between Mexico and the United States.’ You may believe the mainstream media and Trump’s lies when you hear that the wall will be designed to keep illegal immigrants out of the United States, but that is false. The ‘wall’ will actually be encapsulated with thousands of microwave guns- that can track any bird entering the United States and shoot it with harsh microwaves- which destroy the birds ability to fly- and will leave it deceased in under a few hours. I hope this does not shock you too much, after all- if you’ve made it this far In the reading, your entire view on this country has been totally reframed.
The Secrets and Science Behind Starling Murmurations
Individually, a European starling is little more than a common blackbird. That's it. Starlings are short and thick, with dark feathers and long, pointy bills. You've seen them. They're practically everywhere, more than 200 million are in North America alone, singing their chirpy little songs and becoming, to many backyard growers and full-time farmers, a bit on the pesty side.
Collectively, though, starlings transform into something else entirely. Together, in flight, in mesmerizing flocks that sometimes number in the hundreds of thousands, they are a breath-stealing wonder, a pulsating, swooping, living, harmonized whole, seemingly defying the laws of nature while defining nature itself.
Watching a murmuration of starlings in mid-air — that's what the flocking behavior is called, a murmuration — is to experience firsthand the power and mystery of the natural world.
"I think that the core feeling is a sense of awe," says Mario Pesendorfer, a postdoctoral research associate at the Institute of Forest Ecology at the University of Natural Resources and Life Sciences, Vienna. "The spatial scale of something that is moving very rapidly — which we are utterly unable to do — and the visual patterning that occurs when a lot of individuals are doing the same thing . really mesmerizes us."
To scientists like Pesendorfer, murmurations do more than that. They spark curiosity. And they spark scientists like Pesendorfer to figure out how swarming animals — like birds and bees and fish — can better our own lives.
The Secrets Behind Murmurations
In the 1930s, famed ornithologist Edmund Selous suggested that birds moving in murmurations were using some sort of telepathy to transmit their flying intentions. "They must think collectively, all at the same time. a flash out of so many brains," he wrote in his book, "Thought-Transference (or What?) in Birds."
As the years wore on, we found out that's not quite it. In the 1950s, scientists studying insects and fish and other collective animal behavior posited that group movement is more of a stunningly fast response to others in the flock (or the school, or the swarm) rather than some innate mind-reading ability or a command from the group leader.
It's "the rapid transmission of local behavioral response to neighbors" that enables such startling synchronicity, as the authors of a 2015 paper published in the journal Proceedings of the National Academy of Sciences wrote.
"There's two ways that you can elicit large group behavior. You can have the top-down control, where you have some kind of leadership, or some kind of top-down mechanism. Think of a rock show, you have the rock star in the front and he starts clapping his hands, and the whole stadium starts clapping," Pesendorfer says. "But these murmurations are actually self-organized, meaning that it's the individual's little behavioral rules that make it scale up to the large group. In order to understand this behavior, we have to go from the local scale — what is the individual doing, what are the rules that the individual is following? — to the global scale what is the outcome?"
In 2013, a mechanical and aerospace engineer and her team from Princeton collaborated with physicists in Italy to study murmurations. "In a flock with 1,200 birds, it is clear that not every bird will be able to keep track of the other 1,199 birds," Naomi Leonard, the Princeton engineer, said back then, "so an important question is 'Who is keeping track of whom?'"
The Italian physicists used more than 400 photos from several videos to find out, plotting the position and speed of birds as they flocked. From that, they built a mathematical model that identified the optimal number of flock-mates for each bird to track.
Turns out the magic number is seven: Each bird keeps tabs on its seven closest neighbors and ignores all else. Considering all these little groups of seven touch on other individuals and groups of seven, twists and turns quickly spread. And from that, a whole murmuration moves. The scientists' findings were published in the journal PLOS Computational Biology in January 2013.
The Three Things in Control
Though it looks coordinated on a large scale, the individual birds are concerned with only three aspects of their flight and the flight of those around them. These factors have been described in several ways, but they're all very similar. They are, from Pesendorfer:
- An attraction zone: "Which means, in this area, you're going to move toward the next guy."
- A repulsion zone: "Which means, you don't fly into his lane, otherwise you both fall."
- Angular alignment: "So you got to kind of follow his [a bird's neighbor] direction."
"Depending on how you change those three parameters," Pesendorfer says, "you can get everything from those barrel-looking baseballs that you get in ocean fish, to loose-looking insect swarms, to highly, highly organized fish swarms and murmurations. All in those three little parameters."
Scientists believe these birds flock in the first place to confuse and discourage predators, through their sheer numbers, with the noise such a flock makes and, of course, its motion. Some communication between birds may be happening, too, in murmurations — say, pointing out good food sources — while some researchers believe simply keeping warm may be another reason for the murmurations
What may be most stunning to mere mortals is that these birds react so quickly and do so in such synchronization if not immediately, within a couple of flaps of a bird's wing. They move almost as one, in a type of lock-step (or, as it were, lock-flap).
"Birds have a much higher temporal resolution than we do," says Pesendorfer, meaning that birds take in certain information around them and process it much more quickly than humans. "They see much faster than we do."
Using What We Learn From Starlings
Back in 1986, Craig Reynolds, an MIT-trained computer scientist, built computer models of bird flocking and fish schooling in something he called "Boids." These programs provided the basis for lifelike animation in movies, initially (and notably) a swarm of bats in the 1992 Tim Burton film "Batman Returns."
In applications to real life, the ability to understand the behavioral movements of large groups of starlings (or bats or bees or whatever) and to program swarms of robots into making similar movements has amazing possibilities. "We are trying to draw inspiration from biology," George Young, who was the lead author on the paper produced from Leonard's group, told Princeton University back in 2013, "to understand what measures of animal group performance can help us decide what measures we should use when we design responsive behaviors for robots."
An example: Las Cumbres Observatory has 22 robotic telescopes on seven sites around the world that coordinate with each other to function as one big telescope. From the LCO site:
Another example: The emerging field of swarm robotics uses information gleaned from the study of starlings that could, according to the Wyss Institute at Harvard, "enable new approaches for search and rescue missions, construction efforts, environmental remediation, and medical applications."
Swarm robotics also could have use in military applications, like these micro-drones released from fighter aircraft. A swarm of self-driving cars, working together, could help reduce or eliminate traffic jams. The possibilities — cancer-fighting? — are mind-boggling.
All from watching, studying, learning and building on the wondrous flocking of this simple bird.
"As humans who have very complicated decision-making processes, we're not used to looking at simple decision-making processes that scale up to what looks like complex behavior," Pesendorfer says. "These models help us understand these types of patterns."
Watch the video below for an introduction to genetically modified organisms using genetically modified foods as an example. After watching, continue on to the next section.
Learning Lab: Engineer a Crop
So what needs to be done to genetically modify an organism? 'Engineer a Crop' is a digital simulation lab, created by PBS. This resource will walk you through the experience of genetically modifying an organism.
Activity | Complete the Learning Lab.
Together as a class we will be reading an article entitled D.I.Y. Biology, on the Wings of the Mockingjay.
In the article, James Gorman reports on the growing availability of tools to modify organisms, and the possibility that a creature like the bird imagined in the “Hunger Games” series could someday exist.
Activity | As part of our learning, we will be participating in a whole class discussion in our discussion forum.
Once everyone has a chance to reply, please make at least one thoughtful reply in response to what another student wrote.
Lecture 26: Nervous System 3
Download the video from iTunes U or the Internet Archive.
Lecture 21: Development - 1
Lecture 22: Development - 2
Lecture 24: Nervous System 1
Lecture 25: Nervous System 2
Lecture 26: Nervous System 3
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PROFESSOR: So let's get started.
Oh, it's interesting that some of your questions had to do with things that I didn't quite cover in lecture, but that's fine. I'm going to cover them at the beginning of today's lecture.
This is a really important question. How do you know what channel is at-- how do you know what ion a particular channel is conducting? It's actually hard to determine. There are various ways to do it, where you can specifically label the ion, or follow a particular ion, and address whether or not it's getting into a cell or across a membrane, when there's a particular ion channel present. But it's not completely trivial.
One of the things I didn't have time to go through with you, but which is one of the PowerPoints though, is the fact that ion channels are really selective. And they don't conduct ions on the basis of size, OK? So you're not going to get a large ion channel that could accommodate a large ion, also accommodating a small ion. It's not a matter about of just opening up a space.
There are also charge considerations where the ions actually interact with the molecules in the channel, in the actual pore through the membrane. And it's that interaction which selects for a particular ion. But this notion of exactly what ions channels are conducting has been many, many decades of work. And what I've written up here is correct. But if you want to explore it more with me, come and talk during office hours.
And then a number of you started asking me about modulation of neurotransmitters, which I'll talk about in today's lecture. And these are clearly of interest, because many recreational drugs and medications modulate neurotransmitter amounts. And that is how they work.
So for example, some of you might be taking things called SSRIs, specific serotonin re-uptake inhibitors like Prozac, which make you feel less anxious and better about things. And these act by prolonging serotonin activity, by preventing it from being retaken up into cells. And I'll touch on this at the beginning of the lecture. And it takes a while-- is what I've written here-- for these medications to start working, because you're really asking for a rearrangement of the whole synaptic process and the synaptic structure, in order that they can work.
And here is another one. What about amphetamines? Are they neurotransmitters? No. They increase the release of dopamine, which is a neurotransmitter, and they also seem to inhibit re-uptake of dopamine and serotonin is all. I'll talk about re-uptake very briefly in a moment.
For many medications, both-- actually, for many medications, no matter whether or not they affect your brain or other parts of your body, the precise mechanism of action is really not known. There are guesses. There's data. But the precise mechanism is often not known.
So let's use that as a segue into our lecture. I won't have office hours today, due to my schedule. I will have them next Wednesday due to the vacation schedule. And you're welcome to email me in the meantime. All right.
We've been walking through the cells involved in nervous system formation-- the connections between the cells. And now today we're going to finish talking about the connections between the cells and segue into the incredibly complex topic of circuits in the nervous system.
So today, the first thing I want to talk about is regulating synapses. And you remember that we're talking about chemical synapses. And the second thing I want to talk about are circuits.
Is there a problem? Can you hear me OK at the back? Thumbs up. Great. Good.
When I introduced circuits-- when I introduced synapses to you, I told you that one of the reasons that there was this chemical synapse in the midst with a slow chemicals synapse, in the midst of this rapid electrical transmission, was because you could regulate synapses. And that is really what fine tunes us.
It allows us to respond in a graded way to stimuli both from within the body and outside. It allows the body to adapt in ways that are not all or none, where action potentials are all or none. The overall response of the body clearly isn't. It's very nuanced. And all of this has to do with regulating chemical synapses. And that's what we'll talk about for a few moments.
You can regulate chemical synapses by changing the amount of neurotransmitter.
And if you think about this for a moment, if you think about the synapse, there's the neurotransmitter released into the space between the two cells, diffuses across the synaptic cleft, and then does something to the post synaptic cell, potentially to lead to an action potential.
Now if that neurotransmitter stuck around in the space between the cells, it would keep stimulating the postsynaptic cell over and over. And as more neurotransmitter was released, so the postsynaptic cell would be further stimulated. And you would get to a point where the post synaptic neuron was completely over stimulated. And that's clearly not a way to regulate responsiveness to any stimuli. So neurotransmitter does not stay in the synaptic cleft for very long.
So it's changing the amount of neurotransmitter via degradation. Once neurotransmitter is released, in some cases, it's degraded by specific enzymes. For example, in the case of acetylcholine, there's a particular enzyme that breaks down acetylcholine. And if that enzyme is inhibited, you go into respiratory shock. You cannot breathe anymore, because you have to activate and inactivate the muscles via the nerves, as you breathe.
You can also regulate the amount of neurotransmitter by something called re-uptake, sometimes called reabsorption, where the neurotransmitter-- absorb-- tion-- where the neurotransmitter is released. And then it's taken up by the presynaptic cell, which is a frugal way of doing things. It doesn't have to keep synthesizing the neurotransmitter, and that-- so reabsorb-- re-uptake by the presynaptic cell.
And that is the case for serotonin and dopamine.
And then in some cases, you can regulate the synthesis, the amount of neurotransmitter that's being made. And the big class of neurotransmitters regulated in this way are the endorphins, which are a group of peptide neurotransmitters that are the natural opiates of the body, the natural pain regulators of the body. And all of these processes are regulatable both for modulating normal synapses, and also in all cases, for medication targets, for drug targets-- so normal modulation and drug targets.
Let's look at a couple of slides.
Acetylcholine is a neurotransmitter that binds its receptor on the postsynaptic membrane. And after it's done so, acetylcholinesterase, the E here, comes and breaks it down and stops it restimulating the postsynaptic cell.
Many nerve gases-- sarin was one of the famous ones that was used in the Japanese underground some years ago-- inhibit acetylcholinesterase. And in that case, you get a buildup of acetylcholine in the post-- in the synaptic cleft. You get repeated stimulation of the postsynaptic cell. And that leads to, as I said, respiratory paralysis and death.
Our troops overseas have with them vials of atropine. Atropine is a competitive inhibitor of acetylcholine-- binds to the receptor and prevents acetylcholine from binding. And in the case of a nerve gas attack, if you inject yourself with atropine, you'll stop the acetylcholine from working. And you'll be OK. You get a little kind of floppy, but you can survive, because they're ultimate mechanisms of stimulating those nerves. OK.
Here's serotonin, the re-uptake pathway. Serotonin is released as all neurotransmitters, and then it's reabsorbed by the presynaptic cell. And SSRIs, whose mechanism of action is really not understood, do something to block the re-uptake of serotonin. All right.
The other way, clearly, that one could modulate how often synapses are active, or how often the postsynaptic cell is stimulated, is by modulating the receptors. Intuitively, if you have more receptors, the neurotransmitter has more places to bind. It can send a greater signal by changing membrane potential, if you decrease the number of receptors, and so on. And it turns out, if you modify the receptors, if you put phosphate groups on them, sometimes you can also change how well they act.
So the other thing to do to modulate synaptic activity is by changing the receptors. And there are really three ways to do this-- change in number or change in the type-- the subtype of receptor-- where there might be a subtle change in amino acid. Because you are using now a different gene to make the receptor.
You can increase or change the affinity for neurotransmitter. And you can change receptor responsiveness.
All of these three things have got something to do with learning and memory. They have to do with addiction. And all of these changes are slow. They occur over minutes, days, weeks, even. And for some, we understand how these changes occur, but for many, we don't.
The outcome of changing the receptors-- and I see we have a board issue here. So I'm going to put this on-- actually, let me put this board down-- and this board up.
One of the outcomes of changing all of these parameters about the receptors is that over a long period of time, you really change how a synapse works. And you can change how a synapse works through these parameters, by repeatedly stimulating that synapse, OK?
This is what practice does. When you practice your musical instrument, or you practice your biochemistry problems, and you do it over and over, you're changing the synapses that allow you to engage these problems.
And these processes have got names. So let me just complete this. So by changing receptors so that repeated synaptic stimulation-- changes the responsiveness of the synapse-- generally, as I say, through the receptors in this case. OK.
And there are two outputs. One, you can increase the synaptic response. You can make it more likely that there'll be an action potential. And that would take place at excitatory synapses.
And this process is known as a long term potentiation. It's the stuff you want when you're trying to learn something. It's believed to be the way memory works.
You can also decrease the response of a particular synapse, and that would work if it was an inhibitory synapse. And in that case, the process is called long term-- let's just write it out-- long term depression.
Both of these processes have been shown to work in the lab, in culture-- hard to do those experiments on real animals. But it's believed that that's how memory works.
So in your first handout, I've drawn out for you the idea. Here is a normal axon. The presynaptic and the postsynaptic cell-- neurotransmitters released. It engages receptors. And at some frequency, there's an action potential elicited.
If you change-- if you repeatedly stimulate that axon over time-- days, minutes-- you change the receptor spectrum on the postsynaptic cell. And in long term, potentiation responsiveness increases. Whereas in long term depression, you decrease receptor number, or some other parameter, and you lead to decreased responsiveness.
OK. Let us move on to our second topic, which is that of circuits, which refers to multiple connectivities-- multiple synapses forming in a way that is stable, and that can lead to particular outcomes of particular stimuli.
Let's look at your next handout to try to get a sense of where we are. So I've diagrammed this out for you. And I've started here with some kind of sensory neuron, an interneuron, and a motor neuron-- three connected neurons. You could put a lot of these other things called interneurons in the way.
Sensory neurons receive signals. Motor neurons tell things to happen, like muscles to work. And interneurons, of which there can be many, are the connectors between sensory and motor neurons.
There's an input, and there's an output. And what happens in between-- this is a synthesis of what we've talked about over the last couple of lectures. The sensory neuron makes multiple synapses onto the interneuron. They can be excitatory or inhibitory. They're summated.
The interneuron then decides whether to make an action potential or not-- action potential-- yes or no in each case. If it makes an action potential, it sends its signal to the next neuron, the motor neuron. That motor neuron is getting a bunch of inputs-- excitatory and inhibitory. And it, again, has to decide whether or not there's an action potential, OK? So that's the context that puts circuits, where we have been discussing the process of setting up the connections in the nervous system.
The thing about circuits-- and here's a term you should know-- is that they have to do with axon pathfinding. And so let's, for a moment, forget this diagram, which is a diagram of what there is in the adult. And let's think about how these circuits are set up.
The circuits that we have in our brains and then our bodies are of the close to uncountable. I'm not sure we ever will count them in an animal as complex as ourselves. It's been done in caenorhabditis, which has got 1,000 cells-- the little worm we talked about-- it's got 1,000 cells.
And all of the connections in caenorhabditis have been mapped. And they are extremely complex. But that's just a handful of neurons. When you're talking about 10 to the 10th, 10 to the 11th neurons, those connections are enormous.
But we can ask some basic questions, OK? And let's just state it. Neurons are connected to form circuits.
We can say that they're functional circuits, if you like. That is implicit. And the big question is, how do these circuits know where to form?
Or if you like the restatement, how do the neurons know where to go-- know to go and where to connect?
And there are two kind of intuitive answers, both of which turn out to be correct. Either the neurons just go every which way. And if it works, that's retained, and the rest of the connections just are dissolved and go away. And that's true.
But the bigger truth is that the neurons are told where to go. So you can phrase these that the neurons undergo some kind of random process where neurons survive if connections are made.
Or there's some kind of guided process where the neurons are told where to go.
And both of these turn out, after many, many years of work, to be correct.
Let's look at some slides here. This is work from Professor Fee, over in Brain and Cognitive Science. He studies these little birds and their song circuit, which forms and reforms during the life of the bird.
The circuit is complicated. These are not single neurons. They are bundles of neurons. But it's kind of mappable.
And this is one of the circuits. It's got something to do with song within the bird brain. It's not the entire circuit. That's one of the things that's going on here on campus.
But when you start thinking about things like language-- I really like this slide. Because these are activity plots of the brain that can be done in a number of ways by monitoring oxygen uptake, or glucose use. But you can look and see different parts of the brain are active.
And when you think about language-- here are these four parts of the brain. Actually, here is a huge part of the brain used to generate words. Each of these parts of the brain are millions and millions of neurons, which are connected to one another within these regions.
And then each of these regions is connected to one another. And each of those regions is connected to the output, which would be all of your vocal apparatus. And all of this is connected to your auditory apparatus, to your visual system, so that you can read words. They can be processed, and so on.
The connections that give language probably take a very large part of your brain. I would throw out 15% to 20% of your brain is involved in some aspect of language-- receiving, generating, or output. And the circuits there, as I said, are enormous. OK.
So do neurons know where to go? Let me go with you. This isn't on your handout. This is to look on the screen. Do neurons know where to connect?
There was a very famous experiment done by Sperry, some many years ago-- Roger Sperry-- who got a Nobel Prize for his work-- that involved a frog. And it involved figuring out where the neurons in the retina went.
So it turns out, if you look at your eyes, OK, there are neurons that go from your eye back into your brain. The neurons on the side of your nose are called the nasal neurons. And the neurons on the side of you, or the outside of your face, are called temporal neurons.
And what Sperry did was to take an adult frog and rotate the eye 180 degrees so that the nasal neurons would now be on the outside of the head. The temporal neurons would be on the inside of the head, OK? And for a while after the operation, the frog was really confused. But after a while, it actually recovered.
Now let's lay out this-- and the recovery, as I'm going to tell you, told Sperry and the world that neurons were told where to go. So here is the retina depicted as a circle. And here's a part of the brain called the optic tectum, that the neurons connect to. It's the first part of their circuit.
Here are the temporal neurons connecting to the C region of the brain, and the nasal neurons connecting to the R region.
So after this rotation, there were two possibilities. One was that the axons growing out.
So let's just be clear. In this rotation, these axons were severed. They were cut. They had to regrow and find their targets, if they could.
So one possibility would be that the axons would grow out of this retina, and they'd grow everywhere. And they wouldn't make really wrong connections. And things would be a mess.
In actual fact, what really happened was that the nasal neurons, even though they were on the wrong side of the face, found their way to the R region. And the tactile neurons found their way to the C region, just like they had connected to before. And this was a really profound experiment that told investigators that axons knew where to go. And we know the molecular basis of this now, but I'm not going to tell you about it.
In order to understand more about this guidance process, you need to understand a part of the axon that we haven't discussed, and a time in the neurons life that we haven't discussed either. And that is a time when neurons are growing.
Most neuronal growth takes place during embryonic development, but it continues throughout life. And so this is a developmental process, but also in that experiment, that was an adult frog. OK.
So guidance of neurons-- and as we'll discuss, particularly axons-- occurs during development and repair-- and learning as well. We can put that up as well-- during development, repair, and learning. Although I'd say for learning there's a bit of a question mark whether that's true. But I think it's probably true. OK.
And the cell that we need to consider is a committed neuron, which is called a neuroblast. It doesn't matter. But here's your committed neuron.
You have to think back to past lectures-- a neuron that knows that it's going to be a neuron but hasn't decided to-- hasn't become one yet-- hasn't differentiated. It's called a neuroblast. And here it is. It's just a cell body with the nucleus.
And over time, this neuroblast sends out processes that are called neurites. They initially look the same. Soon some of them become dendrites. And one of them becomes an axon-- some neurite, axon, plus dendrite outgrowth.
So you have a cell now with some processes. And one of these is going to be the axon. And that axon grows. And it's during that growth process that it figures out where to go.
The cell body doesn't move. The dendrites don't move. It's the axon that is doing the pathfinding.
So the axon extends and eventually finds its target.
And this extension is a growth process that we'll talk about. OK.
For every-- a nerve-- when we talk about nerves-- there are actually many-- many neurons, many axons. There are bundles of axons. And there is something about the first axon to find a target, that's very important-- the pioneer axon. The first one finds the target. And then others follow-- the same path that lays down a path.
And they form bundles, also called fascicles. And these fascicles together make the nerve.
The part of the axon that's really important for this process is the very tip of the axon, and it has a special name called the growth cone. So the axon tip, or the growth cone, is crucial.
And we can draw it on the board. If we now draw an axon-- and we've blown it up now. So usually we blow up and we lose bits, but now we're not going to lose any bit of it. Here's the axon.
And down the length of the axon are parallel microtubules-- many of them. And these microtubules both stabilize the axon and also transport substances to and from the cell body. So they stabilize the shape of very long axons, and they also transport, like little railway tracks, substances to and from the cell body.
That's not the tip of the axon. At the very tip, the microtubules end, and they interdigitate with these finger-like protrusions, which are very dynamic. That means they change all the time.
And these protrusions protrude because of polymerized actin. And you might be saying, we heard about that already. Yes. You've heard about that in morphogenesis. We've talked about this.
Cell biology is cell biology, whether it's about neurons, or cells in your stomach, or cells in your-- that give rise to the hairs on your head. All of these cells are just cells.
So there are these protrusions at the end. So this whole thing is the axon. But the very end is the growth cone. This very end is the growth cone.
And these protrusions go by the name of filopodia, filamentous, and lamellipodia, more flattened feet. And they protrude because of the polymerization of actin within them. So there's F-actin leads to protrusions.
Well, that's one important thing. And I'll show you a movie in a moment to show you that as an axon grows, it's sending out zillions of these things all the time that are feeling their way around the place. Actually, I'll-- no. I won't show you now, because there's an intervening slide.
But the other thing you should know is that like all cells, there are receptors on the surface of the growth cone that are also sampling what ligands are in the environment. And if the ligands are favorable, they will either stabilize these protrusions and make more of them to take place.
So here are receptors all over the place. This is a receptor. And if receptors contact ligands, then again, you will get F-actin formed. And protrusions will be formed. And they will be stabilized. OK.
The growth cone is paramount to axon outgrowth. There are signals which both attract axons towards them, and signals which repel axons. We can call those, not surprisingly, attractive signals. We'll talk about some in a moment.
And in that case, the growth cone extends. And it extends-- not to beat a dead horse here-- but because F-actin increases or is stabilized. And the flip is that the growth cone can be destabilized and literally collapse under repulsive signals.
The growth cone collapses. And it collapses because F-actin now becomes G globula, or unpolymerized actin, using exactly the same processes that we talked about during the morphogenesis lecture.
Let's look at a couple of slides. You don't have these. So just look on the screen.
This is a cell drawn in Professor Lodish's book. Here's the leading edge of the cell. The direction of the cell is where there is lots of polymerized actin.
This I've just drawn on the board.
And here is an axonal growth code. And I really like this movie. It's a time lapse taken over 10 minutes. And you can see all these things at the end and on the sides-- these protrusions from the cell-- very active.
They're forming. They're disaggregating, forming again and disaggregating as the cell-- those of the lamellipodia and the filopodia-- as the cell is feeling its way through the environment-- trying to find somewhere to go, OK? So this is a real exploratory process by the cell. Good.
What are these guidance signals? Well, this is not a mystery either. Ligands-- we know about receptors. You know about the guidance signals are ligands.
And these ligands, when they're bound to a receptor, lead to signal transduction and axon outgrowth. So ligands-- and we'll put in parentheses, plus receptors-- to signal transduction-- and a change in the growth cone.
There are two kinds of guidance signals that are reasonably separate from one another. They're called short range and long range guidance signals.
Short range signals require contact between the axon and the extracellular matrix, or the axon and another cell. So there's some localized accumulation of a signal, and that has to be directly contacted by the growth cone-- so require axon ECM, or cell contact.
These signals are not diffusible. Therefore-- and they include things like laminin, which is a part of the extracellular matrix, but also an axon guidance signal.
And then there are long range signals, which would be the flip of the short range. These are diffusible. And they can be concentration dependent in their effect.
And we talked about things like this previously when we talked about morphogens-- other ligands that can act at different concentrations in different ways. OK. And an example that I'll explore more with you is the netrin protein.
All right. Let me see what I have here. OK, this is nice. This is on your-- this is your next handout. And this is an assay for short range guidance signals. It's called a stripe assay. And this was how it was found.
What those nasal and temporal retinal neurons grew on-- the idea is you take a plastic dish, and you put stripes of different molecules on the dish. And then you put neurons all the way along one side of the dish. And you look at them. You ask where they grow.
And they'll choose where to grow. And if they like one of the molecules, if they can interact with one of the molecules on the dish, they will grow in particular stripes, and not in other stripes. And that gives you your experiment and control in one dish.
This is what it looks like. So here are the neurons from the nasal side of the retina. And those nasal neurons, which project to the R side of the tectum, grow on our membranes, but not on C membranes, which is where they don't go. You may not have this, but you can go back and look at this later on. All right.
But let's move on now to an example that I want to spend a bit of time on. And the example of a long range signal is that the netrin in the spinal cord.
And what we're going to talk about are two types of neurons, one of which are growing down the spinal cord from the back, more towards the belly, and another type of neuron that's growing more from the belly side of the spinal cord, back towards the back, OK? And those neurons always know where to go. And it turns out they are told where to go by the same signal.
So there are two types of neurons. There are these things called commissural neurons. And they grow ventrally, or down, towards something called the floor plate. I'll show you in the diagram. And then there are these other ones called trochlear neurons that grow dorsally, or up. And they grow away from this thing called the floor plate.
And it turns out, using an explant assay, that I'll go through with you in your slides-- but you should understand-- it was found that a single molecule called netrin, which is a secreted ligand, a secreted protein, that's expressed in the floor plate-- which we'll talk about in a moment-- is attractive for the commissural neurons and repulsive for the trochlear neurons.
And it also turns out, as we'll go through in a moment, that this has to do with different receptors and different receptor dimers, which bind the same ligand. And so here there is something called, for the commissural neurons, there is something called a DCC-- DCC receptor dimer.
And for the trochlear neurons, there is a DCC UNC5 receptor pair. And this will not mean much to you, but now you can write it down. And then you can go through your slides. And you'll have a reference point on right with you. OK.
So here is the diagram. The cell bodies of the commissural neurons are up in this region of the spinal cord called the roof plate. It's the top of the spinal cord.
And on the bottom of the spinal cord, near your belly, there is a cone-shaped group of cells that forms this thing called the floor plate. The floor plate doesn't actually make neurons. It turns out to be a really important source of signals. It's an organizer, if you like.
And it not only organizes these axons in the spinal cord, it actually also organizes your midline. And it's one of the reasons, if you're missing the midline of the body, things go wrong. It's because the floor plates are not there.
So the floor plate is an organizer. They are the commissural neurons growing towards it. And here are the trochlear neurons growing away from the floor plate.
This is what it looks like if you do an immunostain. The cell bodies are in red. And here are the commissural neurons coming down in the spinal cord.
And this is a section through the spinal cord, OK? You've cut through-- cut through at the waist and then turned the section on its side. So you're looking into the spinal cord, which would be coming out in its length from the board-- from the screen.
All right. Here's an explant assay to figure out whether or not that floor plate has got something to do with the direction that those commissural neurons grow. So on your handout, the idea was to take a piece of dorsal spinal cord that hadn't started to send neurons out yet, and to culture it together in the laboratory, in a plastic dish, with some fluid nutrients, and so on, and ask what happened. And if you did that, that dorsal spinal cord sent out neurons towards the floor plate.
On the other hand, you can see that that experiment was specific, because if you put the dorsal spinal cord together with some roof plate, nothing happened. There was no outgrowth. So there was something special about this floor plate that elicited that commissural acts on outgrowth. And the idea is that the floor plate was attracting the commissural axons.
This is what it really looks like. Here's a chunk of dorsal spinal cord and floor plate. And here are the growing axons. And here's the control experiment. All right.
So what is the protein involved? Well, the idea was that it was something in the floor plate. And it was really hard to find this, because there's not much of it.
Professor Tessier-Lavigne, who is now president of Rockefeller University, but at the time he was running a research laboratory, and he and many undergraduates, and graduate students, and post-docs, and so on, went ahead and dissected many, many little floor plates. And they also found that the brain of the chicken contained the same kind of activity.
So they dissected out many thousands-- I believe it was 35,000-- chick brains and spinal cords. And they did biochemistry on this material. And they used the explant assay that I just showed you, where instead of the floor plate, you'd have a little pellet of material in which you had soaked the material that you've purified by biochemistry, from your smushed up, dissected brains.
And from this-- it was really successful-- from this, they got a single protein. Here's the RNA for the protein. That's right expressed in the floor plate. That's what the white is. That's the RNA. This is an in situ hybridisation. And they called it netrin.
Netrin protein diffuses away from the floor plate, but it's still mostly on this ventral side of the spinal cord. And you could show that netrin was important, because if you meet a mouse that lacked netrin-- here's the mouse that lacks netrin-- the commissural neurons go all over the place. They really don't know where to go. All right.
The netrin receptors, as I drew on the board-- you can look on your last handout-- are two-fold. One of them are called DCC, the tyrosine kinases. They also activate GTPases and do some other signal transduction.
And when netrin binds to a dimer of DCC, you get F-actin that's made. Microtubules grow. And the growth cone extends.
On the other hand, when you get this hetero dimer DCC and UNC5, or a different homodimer, you get cytoskeletal remodeling, G-actin made, and the growth cone collapses. OK. Close enough. We'll stop there.
Are these birds in video real? What are they called? - Biology
B irds played a major role in creating awareness of pollution problems. Indeed, many people consider the modern environmental movement to have started with the publication in 1962 of Rachel Carson's classic Silent Spring, which described the results of the misuse of DDT and other pesticides. In the fable that began that volume, she wrote: "It was a spring without voices. On the mornings that had once throbbed with the dawn chorus of robins, catbirds, doves, jays, wrens, and scores of other bird voices there was now no sound only silence lay over the fields and woods and marsh." Silent Spring was heavily attacked by the pesticide industry and by narrowly trained entomologists, but its scientific foundation has stood the test of time. Misuse of pesticides is now widely recognized to threaten not only bird communities but human communities as well.
The potentially lethal impact of DDT on birds was first noted in the late 1950s when spraying to control the beetles that carry Dutch elm disease led to a slaughter of robins in Michigan and elsewhere. Researchers discovered that earthworms were accumulating the persistent pesticide and that the robins eating them were being poisoned. Other birds fell victim, too. Gradually, thanks in no small part to Carson's book, gigantic "broadcast spray" programs were brought under control.
But DDT, its breakdown products, and the other chlorinated hydrocarbon pesticides (and nonpesticide chlorinated hydrocarbons such as PCBs) posed a more insidious threat to birds. Because these poisons are persistent they tend to concentrate as they move through the feeding sequences in communities that ecologists call "food chains." For example, in most marine communities, the living weight (biomass) of fish-eating birds is less than that of the fishes they eat. However, because chlorinated hydrocarbons accumulate in fatty tissues, when a ton of contaminated fishes is turned into 200 pounds of seabirds, most of the DDT from the numerous fishes ends up in a relatively few birds. As a result, the birds have a higher level of contamination per pound than the fishes. If Peregrine Falcons feed on the seabirds, the concentration becomes higher still. With several concentrating steps in the food chain below the level of fishes (for instance, tiny aquatic plants crustacea small fishes), very slight environmental contamination can be turned into a heavy pesticide load in birds at the top of the food chain. In one Long Island estuary, concentrations of less than a tenth of a part per million (PPM) of DDT in aquatic plants and plankton resulted in concentrations of 3-25 PPM in gulls, terns, cormorants, mergansers, herons, and ospreys.
"Bioconcentration" of pesticides in birds high on food chains occurs not only because there is usually reduced biomass at each step in those chains, but also because predatory birds tend to live a long time. They may take in only a little DDT per day, but they keep most of what they get, and they live many days.
The insidious aspect of this phenomenon is that large concentrations of chlorinated hydrocarbons do not usually kill the bird outright. Rather, DDT and its relatives alter the bird's calcium metabolism in a way that results in thin eggshells. Instead of eggs, heavily DDT-infested Brown Pelicans and Bald Eagles tend to find omelets in their nests, since the eggshells are unable to support the weight of the incubating bird.
Shell-thinning resulted in the decimation of the Brown Pelican populations in much of North America and the extermination the Peregrine Falcon in the eastern United States and southeastern Canada. Shell-thinning caused lesser declines in populations of Golden and Bald Eagles and White Pelicans, among others. Similar declines took place in the British Isles. Fortunately, the cause of the breeding failures was identified in time, and the use of DDT was banned almost totally in the United States in 1972.
The reduced bird populations started to recover quickly thereafter, with species as different as ospreys and robins returning to the pre-DDT levels of breeding success in a decade or less. Furthermore, attempts to reestablish the peregrine in the eastern United States using captive-reared birds show considerable signs of success. Brown Pelican populations have now recovered to the extent that the species no longer warrants endangered status except in California. The banning of DDT has helped to create other pesticide problems, however. The newer organophosphate pesticides that to a degree have replaced organochlorines, such as parathion and TEPP (tetraethyl pyrophosphate), are less persistent so they do not accumulate in food chains. They are, nonetheless, highly toxic. Parathion applied to winter wheat, for instance, killed some 1,600 waterfowl, mostly Canada Geese, in the Texas panhandle in 1981.
Unfortunately, however, DDT has recently started to become more common in the environment again its concentration in the tissues of starlings in Arizona and New Mexico, for example, has been increasing. While the source of that DDT is disputed, what is certain is that DDT has been shown to be present as a contaminant in the widely used toxin dicofol (a key ingredient in, among others, the pesticide Kelthane). Dicofol is a chemical formed by adding single oxygen atoms to DDT molecules. Unhappily, not all the DDT gets oxygenated, so that sometimes dicofol is contaminated with as much as 15 percent DDT
Overall, the 2.5 million pounds of dicofol used annually in pesticides contain about 250 thousand pounds of DDT. In addition, little is known about the breakdown products of dicofol itself, which may include DDE, a breakdown product of DDT identified as the major cause of reproductive failure in several bird species. Finally, DDT itself may still be in use illegally in some areas of the United States, and migratory birds such as the Black-crowned Night-Heron may be picking up DDT in their tropical wintering grounds (where DDT application is still permitted). Unhappily tropical countries are becoming dumping grounds for unsafe pesticides that are now banned in the United States. As the end of the century approaches, the once hopeful trend may be reversing, so that DDT and other pesticides continue to hang as a heavy shadow over many bird populations.
Copyright ® 1988 by Paul R. Ehrlich, David S. Dobkin, and Darryl Wheye.