Role of endorphins discovered
In the 1960s, nuerochemist Choh Hao Li at the University of California in San Francisco was investigating the pituitary gland for substances that aided in the metabolism of fat. It was hard to get enough of this substance, though, so he acquired about 500 dried camel pituitaries. But the camels had none of this fat-metaboliser. Li isolated another amino acid substance from the camel pituitary, beta-endorphin, but it didn't play into the questions he was asking and he put it in storage.
In 1973, research teams in Sweden, Baltimore, and New York independently found that the brain has special receptors that interact with opiates such as morphine. Strong opiates tended to bind better to these sites than weak ones. This seemed odd. Why would human brains around the world have a receptor for morphine, the product of flowers that originated in the Middle East?
In 1975, John Hughes and Hans Kosterlitz published their discovery of a small amino-acid molecule in the brains of pigs. They called this molecule "enkephalin"(meaning "in the head"). It had some of the qualities of morphine, which helped answer the question of why the brain had receptors for morphine. Hughes thought they might be able to use enkephalin in painkillers that were not as addictive as morphine. They tried this idea out in the lab and were disheartened to find that the reverse was true: The painkilling power was weak, but it was extremely addictive.
Back in San Francisco, Li realized that the beta-endorphin he had isolated contained enkephalin. Now he had a question to ask about it: Did it have something to do with pain perception? When Li injected the substance into the brain, he found it was 48 times more powerful than morphine; injected in the vein it was 3 times as powerful. And also addictive.
This research allowed neuroscientists to conclude that the brain has receptors for painkillers which the pituitary releases under great stress. If an artificial painkiller such as morphine is given, it occupies more of the pain receptors in the brain; however, less natural painkiller is released. Then, when the artificial source is taken away, there are more empty pain receptors, causing the craving for narcotics and a withdrawal response.