With this background, we can understand the story of the neurochemistry of stress-induced analgesia that began in the early 1970s. It was a time of the hippie culture in America and the rest of the world. The young men and women in the West had then discovered the joys of opiates and the pleasures to be derived from them. Naturally, the leading-edge scientists of that time wanted to know how the various drugs like heroin, morphine, and opium worked.
All those drugs have a fairly similar chemical structure and are made by plants in the same way. In a surprising scientific race, three groups of scientists almost simultaneously reported that these drugs worked by binding to receptors in the brain. It turns out that these receptors are located in areas where the brain processes pain perception. As these drugs bind to the receptors, they activate the descending projections from the brain that, in turn, blunt the sensitivity of the pain neuron X (what we called Gate 1 in our discussion in the previous section). Net result of the opiates—pain is blocked!
Just as you digest this explanation, a puzzle hits you like a meteor. Why should the brain have receptors for chemicals made by some plants? The obvious answer comes flooding in: there must be similar chemicals made by our body. The body must make some kind of morphine.
The story lurches forward as enthusiastic teams of neu-rochemists rushed to discover the endogenous opiates. It would be a tremendous achievement to find the body’s natural painkillers. Going further, if synthetic versions of these body painkillers could be made without being addictive, fame and fortune would surely follow. In the ensuing decade, competing teams of scientists found exactly what they were looking for—the compounds made by the body (endogenous compounds) with chemical structure closely linked to the plant opiates.
Three classes of chemicals were discovered— enkephalins, dynorphins and endorphins (abbreviation for endogenous morphine). The opiate receptors of the brain were found to bind to these endogenous chemicals just as expected. Furthermore, these opiates were synthesized and released in that part of the brain which processes pain. The rest as they say is history.
We all know about the famed runners high—that irrational feeling of euphoria and lack of pain that comes at the 30- or 40-minute mark into strenuous, exercise. During exercise, beta-endorphin pours out of the pituitary gland. Around the 30-minute mark enough of it builds up in the bloodstream to cause analgesia. Enkephalins are also activated in the brain and spine. They activate the descending pathways to shut out the action of neuron X. All sorts of other stressors produce similar effects.
Surgery, childbirth, examinations, and exposure to cold all cause the same analgesia. From an evolutionary point of view, this is another example of a system that works as expected. As an animal experiencing the stress of being chased by a predator or involved in a dominance fight with another member of the family, it makes sense that a system has evolved to suppress the pain. Now would be a wrong time to feel the aching joint or the pain from the sharp claws. So, where is the problem?
Fortunately, this is one system where no one has shown any problem from repeated activation. That is one less excuse for couch potatoes for not exercising. Repeated releases of beta-endorphins have no ill-effects and the exercise will do you a lot of good.
Therefore, I urge all the readers to stop reading go and do their exercise before continuing! The only bad news in the release of the body’s opiates is that it does not go on forever. The secretions diminish and the pain returns after a while. This makes sense, as pain is one of the body’s major signalling mechanisms when something is wrong. It would not make sense for our body to turn off the pain signal coming from a broken bone. So, the pain will return after the activity of the opiates is diminished.