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Endorphins ("endogenous morphine") are endogenous opioid peptides that function as neurotransmitters. They are produced by the pituitary gland and the hypothalamus in vertebrates during exercise, excitement, pain, spicy food consumption, love, and sexual activity, and they resemble the opiates in their abilities to produce analgesia and a feeling of well-being.
The term 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 a feeling of exhilaration that can be brought on by pain, danger, or other forms of stress, supposedly due to the influence of endorphins. When a nerve impulse reaches the spinal cord, endorphins that prevent nerve cells from releasing more pain signals are released.
Opioid neuropeptides were first discovered in 1974 by two independent groups of investigators:
Beta-endorphin (β-endorphin) is released into blood from the pituitary gland and into the spinal cord and brain from hypothalamic neurons. The β-endorphin that is released into the blood cannot enter the brain in large quantities because of the blood–brain barrier, so the physiological importance of the β-endorphin that can be measured in the blood is far from clear. β-endorphin is a cleavage product of pro-opiomelanocortin (POMC), which is also the precursor hormone for adrenocorticotrophic hormone (ACTH). The behavioural effects of β-endorphin is exerted by its actions in the brain and spinal cord, and it is presumed that the hypothalamic neurons are the major source of β-endorphin at those sites. In situations where the level of ACTH is increased (e.g., Cushing’s Syndrome), the level of β-endorphin also increases slightly.
β-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-Opioid receptors are the main receptor through which morphine acts. In the classical sense, μ opioid receptors are presynaptic, and inhibit neurotransmitter release. Through that 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 can lead to aberrant synaptic plasticity, which can cause dependency. 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. Also, receptors are often found at postsynaptic locations as well as at presynaptic locations.
Scientists sometimes debate whether specific activities release measurable levels of endorphins. Much of the current data comes from animals 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 central nervous system. 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.
A publicized, putative effect of endorphins is the so-called "runner's high", which is said to occur when people exercise so strenuously that their bodies reach the threshold of endorphin release. Endorphins are released during long, continuous workouts of moderate to high intensity, corresponding to prolonged physical stress. This also corresponds with the time that the muscles use up their stored glycogen. The presence of endorphins would presumably mitigate pain sensation by negatively regulating pain-carrying signals from nociceptive neurons in the spinal cord. Notably, such analgesic effects of endorphins could potentially increase the likelihood of injury, as pain sensation could be more easily ignored. Experiencing a runner's high has also been known to cause feelings of euphoria. Although it is called a "runners" high, the effect can occur anytime that people engage in any strenuous exercise or activity, not just running.
A runner's high has been suggested to have evolutionary roots based on the theory that it helped with the survival of early humans. Current African tribes make use of a runner's high when they are conducting persistence hunting. This is a method in which tribesman hunt an animal and track it for miles, eventually killing it due to its greatly increased vulnerability because it became completely physically exhausted.
In 2008, researchers in Germany reported on the mechanisms that cause a runner's high to occur. Using PET scans, combined with recently available chemicals that reveal endorphins in the brain, they were able to compare runners’ brains before and after a run.
Previous research on the role of endorphins, in producing a runner's high, included trying to understand the mechanisms at work; that data seemed to demonstrate that the "high" comes from completing a physical 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 for several reasons:
Endorphins are known to play a role in depersonalization disorder. The opioid antagonists naloxone and naltrexone have both been proven to be successful in treating depersonalization. To quote a 2001 naloxone study, "In three of 14 patients, depersonalization symptoms disappeared entirely and seven patients showed a marked improvement. The therapeutic effect of naloxone provides evidence for the role of the endogenous opioid system in the pathogenesis of depersonalization."
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.
A placental tissue of fetal origin — i.e., the syncytiotrophoblast — excretes beta-endorphins into the maternal blood system from the 3rd month of pregnancy. A recent study proposes an adaptive background for this phenomenon. The authors argue that fetuses make their mothers endorphin-dependent then manipulate them to increase nutrient allocation to the placenta. Their hypothesis predicts that: (1) anatomic position of endorphin production should mirror its presumed role in foetal-maternal conflict; (2) endorphin levels should co-vary positively with nutrient carrying capacity of maternal blood system; (3) postpartum psychological symptoms (such as postpartum blues, depression, and psychosis) in humans are side-effects of this mechanism that can be interpreted as endorphin-deprivation symptoms; (4) shortly after parturition, placentophagy could play an adaptive role in decreasing the negative side-effects of foetal manipulation; (5) later, breast-feeding-induced endorphin excretion of the maternal pituitary saves the mother from further deprivation symptoms. These predictions appear to be supported by empirical data.
From the words ἔνδον / Greek: éndon meaning "within" (endogenous, ἐνδογενής / Greek: endogenes, "proceeding from within") and morphine, from Morpheus (Μορφεύς / Ancient Greek: Morpheús, the god of sleep in the Greek mythology, thus 'endo(genous) (mo)rphine’.