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Endorphins are endogenous opioid biochemical compounds. They are polypeptides produced by the pituitary gland and the hypothalamus in vertebrates, and they resemble the opiates in their abilities to produce analgesia and a sense of well-being. In other words, they might work as "natural pain killers." Using drugs may increase the effects of the endorphins.
The term "endorphin" implies a pharmacological activity (analogous to the activity of the corticosteroid category of biochemicals) as opposed to a specific chemical formulation. It consists of two parts: endo- and -orphin; these are short forms of the words endogenous and morphine, intended to mean "a morphine-like substance originating from within the body." 
The term endorphin rush has been adopted in popular speech to refer to feelings of exhilaration brought on by pain, danger, or other forms of stress, supposedly due to the influence of endorphins. However, this term does not occur in the medical literature.
Additional recommended knowledge
Opioid neuropeptides were first discovered in 1975 by two independent groups of investigators.
Mechanism of action
Beta-endorphin is released into the blood (from the pituitary gland) and into the spinal cord and brain from hypothalamic neurons. The beta-endorphin that is released into the blood cannot enter the brain in large quantities because of the blood-brain barrier. The physiological importance of the beta-endorphin that can be measured in the blood is far from clear: beta-endorphin is a cleavage product of POMC which is the precursor hormone for adrenocorticotrophic hormone (ACTH). The behavioural effects of beta-endorphin are exerted by its actions in the brain and spinal cord, and probably the hypothalamic neurons are the major source of beta-endorphin at these sites. In situations where the level of ACTH is increased (e.g. Addison disease), the level of endorphins also increases slightly.
Beta-endorphin has the highest affinity for the μ1-opioid receptor, slightly lower affinity for the μ2- and δ-opioid receptors and low affinity for the κ1-opioid receptors. μ-receptors are the main receptor through which morphine acts. Classically, μ-receptors are presynaptic, and inhibit neurotransmitter release; through this mechanism, they inhibit the release of the inhibitory neurotransmitter GABA, and disinhibit the dopamine pathways, causing more dopamine to be released. By hijacking this process, exogenous opioids cause inappropriate dopamine release, and lead to aberrant synaptic plasticity which causes addiction. Opioid receptors have many other and more important roles in the brain and periphery however, modulating pain, cardiac, gastric and vascular function as well as possibly panic and satiation, and receptors are often found at postsynaptic locations as well as presynaptically.
Scientists debate whether specific activities release measurable levels of endorphins. Much of the current data comes from animal models which may not be relevant to humans. The studies that do involve humans often measure endorphin plasma levels, which do not necessarily correlate with levels in the CNS. Other studies use a blanket opioid antagonist (usually naloxone) to indirectly measure the release of endorphins by observing the changes that occur when any endorphin activity that might be present is blocked.
Another widely publicized effect of endorphin production is the so-called "runner's high", which is said to occur when strenuous exercise takes a person over a threshold that activates endorphin production. Endorphins are released during long, continuous workouts, when the level of intensity is between moderate and high, and breathing is difficult. This also corresponds with the time that muscles use up their stored glycogen and begin functioning with only oxygen. Workouts that are most likely to produce endorphins include running, swimming, cross-country skiing, long distance rowing, bicycling, weight lifting, aerobics, or playing a sport such as basketball, football (soccer), or American football.
However, some scientists question the mechanisms at work, their research possibly demonstrating the high comes from completing a challenge rather than as a result of exertion. Studies in the early 1980s cast doubt on the relationship between endorphins and the runner's high. There were a couple of reasons for this doubt.
A study in 2004 by Georgia Tech found that runner's high might be caused by the release of another naturally produced chemical, the endocannabinoid anandamide. Anandamide is similar to the active chemical, THC, found in marijuana. The authors suggest that the body produces this chemical to deal with prolonged stress and pain from strenuous exercise, similar to the original theory involving endorphins. However, the release of anandamide was not reported with the cognitive effects of the runner’s high; this suggests that anandamide release may not be significantly related to runner's high.
In 1999, clinical researchers reported that inserting acupuncture needles into specific body points triggers the production of endorphins. In another study, higher levels of endorphins were found in cerebrospinal fluid after patients underwent acupuncture. In addition, naloxone appeared to block acupuncture’s pain-relieving effects. However, skeptics say that not all studies point to that conclusion, and that in a trial of chronic pain patients, endorphins did not produce long-lasting relief. Endorphins may be released during low levels of pain and physical stimulation when it lasts over 30 minutes. Questions remain as to whether the prolonged low level of pain stimulation as in Capsaicin, acupuncture and running or physical activity alone are the threshold that activates endorphin release.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Endorphin". A list of authors is available in Wikipedia.|