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International Journal of Molecular... Dec 2020β-Endorphins are peptides that exert a wide variety of effects throughout the body. Produced through the cleavage pro-opiomelanocortin (POMC), β-endorphins are the... (Review)
Review
β-Endorphins are peptides that exert a wide variety of effects throughout the body. Produced through the cleavage pro-opiomelanocortin (POMC), β-endorphins are the primarily agonist of mu opioid receptors, which can be found throughout the body, brain, and cells of the immune system that regulate a diverse set of systems. As an agonist of the body's opioid receptors, β-endorphins are most noted for their potent analgesic effects, but they also have their involvement in reward-centric and homeostasis-restoring behaviors, among other effects. These effects have implicated the peptide in psychiatric and neurodegenerative disorders, making it a research target of interest. This review briefly summarizes the basics of endorphin function, goes over the behaviors and regulatory pathways it governs, and examines the variability of β-endorphin levels observed between normal and disease/disorder affected individuals.
Topics: Animals; Behavior; Behavior, Animal; Brain; Energy Metabolism; Humans; Inflammation; Stress, Physiological; beta-Endorphin
PubMed: 33396962
DOI: 10.3390/ijms22010338 -
Neuroscience Aug 2022A possible role for the brain β-endorphin system in memory modulation was proposed by Ivan Izquierdo more than 30 years ago. Along with pharmacologic evidence of the... (Review)
Review
A possible role for the brain β-endorphin system in memory modulation was proposed by Ivan Izquierdo more than 30 years ago. Along with pharmacologic evidence of the effects of morphine and naloxone administered immediately after training in avoidance tasks and with the demonstration of medial-basal hypothalamus β-endorphin release after novelty detection, it was hypothesized that an endogenous opioid state present in the labile period of consolidation will be part of the memory of the newly acquired information. The fact that pre-test novelty exposure, through release of β-endorphin, or the injection of opioids facilitate retrieval supports that. The mechanisms through which novelty exerts its retrieval-enhancing effect were studied; evidence that several forms of amnesia induced by post-training treatments are due to unavailability of retrieval and not to a storage deficit, challenging the memory consolidation framework is discussed. In this review some of the original papers in the subject are revisited. Recent studies on the memory beneficial effects of novelty, both in animal models and in humans, indicate this is line of investigation is worth of pursuing and demonstrate the importance of the seminal work of Ivan Izquierdo in the field of memory modulation.
Topics: Animals; Avoidance Learning; Brain; Humans; Memory; Morphine; Naloxone; beta-Endorphin
PubMed: 35183689
DOI: 10.1016/j.neuroscience.2022.02.014 -
Pain Medicine (Malden, Mass.) Jan 2019Chronic low back pain (CLBP) is usually quantified using the visual analog scale (VAS). However, the VAS is a subjective measure and prone to reporting bias, therefore... (Review)
Review
BACKGROUND
Chronic low back pain (CLBP) is usually quantified using the visual analog scale (VAS). However, the VAS is a subjective measure and prone to reporting bias, therefore making it difficult to differentiate patients with true pain from those seeking to obtain secondary gain. This study aimed to evaluate the feasibility of using plasma β-endorphin as an objective biomarker for CLBP.
METHODS
We searched PubMed, Embase, and the Cochrane Library for randomized trials that compared treatment vs sham procedures for patients with CLBP. Changes in VAS and β-endorphin levels between baseline and final evaluations were assessed for the treatment and control groups. A meta-regression model was developed to evaluate the association between the β-endorphin level and VAS.
RESULTS
We included data from seven trials involving 375 patients. There was no significant difference in VAS scores and β-endorphin levels between both groups at baseline. At final evaluation, the treatment group demonstrated significantly greater improvements in VAS scores and an increased β-endorphin level compared with the control group. The change in the plasma β-endorphin level may be a surrogate marker of treatment response for patients with CLBP (explanatory power: 80%). The plasma β-endorphin level might be rarely affected by sham procedures. For patients with CLBP, the baseline β-endorphin level may reflect the intensity of CLBP (explanatory power: 66%).
CONCLUSIONS
A change in plasma β-endorphin level may be a surrogate marker of the treatment response for patients with CLBP. Advancements in β-endorphin measurements may help us better quantify pain intensity.
Topics: Chronic Pain; Humans; Low Back Pain; Pain Measurement; Randomized Controlled Trials as Topic; Treatment Outcome; beta-Endorphin
PubMed: 30256990
DOI: 10.1093/pm/pny186 -
Acta Anaesthesiologica Scandinavica Jan 1997We have known the endogenous opioid peptide beta-endorphin for 20 years. Surprisingly, our knowledge of the physiological role of this peptide and its receptors in... (Review)
Review
We have known the endogenous opioid peptide beta-endorphin for 20 years. Surprisingly, our knowledge of the physiological role of this peptide and its receptors in modulation of pain perception is still fragmentary. Whereas most studies have tried to elucidate the physiological role of beta-endorphin by reversing evoked responses by the opioid antagonist naloxone, this review focuses on quantification of release of beta-endorphin in the brain as the approach to define physiological and pathophysiological roles of beta-endorphin in relation to nociception. Using a lateral ventricle-cisterna magna perfusion model in the anesthetized rat, it was shown that depolarization of neurons in the arcuate nucleus of the hypothalamus, where beta-endorphin in produced, was followed by release of beta-endorphin to the cerebrospinal fluid compartment. Intense activation of spinal nociceptive pathways by intrathecal capsaicin injections also led to beta-endorphin release. It is concluded that there may still be good reason to quantify beta-endorphin in human cerebrospinal fluid to elucidate the role of beta-endorphin in pain perception.
Topics: Animals; Brain; Capsaicin; Electric Stimulation; Excitatory Amino Acid Agonists; Humans; N-Methylaspartate; Pain; beta-Endorphin
PubMed: 9061096
DOI: 10.1111/j.1399-6576.1997.tb04627.x -
Progress in Neurobiology Sep 2008Although drugs of abuse have different acute mechanisms of action, their brain pathways of reward exhibit common functional effects upon both acute and chronic... (Review)
Review
Although drugs of abuse have different acute mechanisms of action, their brain pathways of reward exhibit common functional effects upon both acute and chronic administration. Long known for its analgesic effect, the opioid beta-endorphin is now shown to induce euphoria, and to have rewarding and reinforcing properties. In this review, we will summarize the present neurobiological and behavioral evidences that support involvement of beta-endorphin in drug-induced reward and reinforcement. Currently, evidence supports a prominent role for beta-endorphin in the reward pathways of cocaine and alcohol. The existing information indicating the importance of beta-endorphin neurotransmission in mediating the reward pathways of nicotine and THC, is thus far circumstantial. The studies described herein employed diverse techniques, such as biochemical measurements of beta-endorphin in various brain sites and plasma, and behavioral measurements, conducted following elimination (via administration of anti-beta-endorphin antibodies or using mutant mice) or augmentation (by intracerebral administration) of beta-endorphin. We suggest that the reward pathways for different addictive drugs converge to a common pathway in which beta-endorphin is a modulating element. Beta-endorphin is involved also with distress. However, reviewing the data collected so far implies a discrete role, beyond that of a stress response, for beta-endorphin in mediating the substance of abuse reward pathway. This may occur via interacting with the mesolimbic dopaminergic system and also by its interesting effects on learning and memory. The functional meaning of beta-endorphin in the process of drug-seeking behavior is discussed.
Topics: Animals; Behavior, Animal; Conditioning, Psychological; Euphoria; Humans; Reinforcement, Psychology; Substance-Related Disorders; beta-Endorphin
PubMed: 18602444
DOI: 10.1016/j.pneurobio.2008.06.003 -
Sports Medicine (Auckland, N.Z.) Jul 1997beta-Endorphin, a 31-amino-acid peptide, is primarily synthesised in the anterior pituitary gland and cleaved from pro-opiomelanocortin, its larger precursor molecule.... (Review)
Review
beta-Endorphin, a 31-amino-acid peptide, is primarily synthesised in the anterior pituitary gland and cleaved from pro-opiomelanocortin, its larger precursor molecule. beta-Endorphin can be released into the circulation from the pituitary gland or can project into areas of the brain through nerve fibres. Exercise of sufficient intensity and duration has been demonstrated to increase circulating beta-endorphin levels. Previous reviews have presented the background of opioids and exercise and discussed the changes in beta-endorphin levels in response to aerobic and anaerobic exercise. The present review is to update the response of beta-endorphin to exercise. This review suggests that exercise-induced beta-endorphin alterations are related to type of exercise and special populations tested, and may differ in individuals with health problems. Additionally, some of the possible mechanisms which may induce beta-endorphin changes in the circulation include analgesia, lactate or base excess, and metabolic factors. Based on the type of exercise, different mechanisms may be involved in the regulation of beta-endorphin release during exercise.
Topics: Animals; Exercise; Humans; beta-Endorphin
PubMed: 9257407
DOI: 10.2165/00007256-199724010-00002 -
Anesthesia Progress 1991Beta-endorphin is a peptide with morphine-like effects produced primarily in the anterior lobe of the pituitary gland. After its cleavage from the parent molecule,... (Review)
Review
Beta-endorphin is a peptide with morphine-like effects produced primarily in the anterior lobe of the pituitary gland. After its cleavage from the parent molecule, proopiomelanocortin, beta-endorphin is circulated via the blood stream to interact with specific opioid receptors located throughout the body. The peptide produces analgesia by inhibiting the firing of peripheral somatosensory fibers. It also affects other senses, such as vision, hearing, and smell. Whereas the ability to increase beta-endorphin secretion during times of surgical stress is positively correlated with amelioration of pain, the administration of exogenous opioids, such as fentanyl, reduces plasma beta-endorphin. Decreased beta-endorphin concentrations may play a role in trigeminal neuralgia, migraine headache, and rheumatoid arthritis.
Topics: Humans; Nociceptors; Pain; beta-Endorphin
PubMed: 1814247
DOI: No ID Found -
Biomedicine & Pharmacotherapy =... 1993Calcitonin is a peptide hormone secreted by the C-cells of the thyroid gland. This hormone mainly acts in preventing bone resorption. Furthermore, calcitonin is involved... (Review)
Review
Calcitonin is a peptide hormone secreted by the C-cells of the thyroid gland. This hormone mainly acts in preventing bone resorption. Furthermore, calcitonin is involved in other biological actions, and in particular it is able to relieve pain independently of its peripheral effects on bone. Here, we examine the possible mechanisms of calcitonin-induced analgesia, with particular regard to the opioid system involvement. Several studies in animals and in humans demonstrate that calcitonin increases plasma beta-endorphin levels, acting at the hypothalamic and/or at the pituitary level, either directly or indirectly, through monoaminergic neurotransmitters. However, this calcitonin-induced beta-endorphin release has not always been observed. These different results are discussed, and a possible implication of sex and/or calcitonin dose employed has been examined. We conclude that the analgesic effects of calcitonin are multifactorial, and beta-endorphin plays its own specific role.
Topics: Analgesics; Animals; Calcitonin; Humans; beta-Endorphin
PubMed: 8061253
DOI: 10.1016/0753-3322(93)90079-z -
Alcohol (Fayetteville, N.Y.) 1988"Reinforcing" effects are ascribed to endogenous opioids, particularly to the pro-opiomelanocortin (POMC)-derived beta-endorphin 1-31, the most potent opiate-active... (Review)
Review
"Reinforcing" effects are ascribed to endogenous opioids, particularly to the pro-opiomelanocortin (POMC)-derived beta-endorphin 1-31, the most potent opiate-active substance. Alcohol induces variations in the genetic processing of the precursor POMC and of beta-endorphin at different levels. Studies focused on changes in POMC gene expression (mRNA quantitation) and post-translational processing. Chronic alcohol intake significantly reduces POMC mRNA in the lobes of the pituitary. In inbred strains of mice, genotypic differences are seen in post-translational processing of hypothalamic beta-endorphin, thus inducing differences in alcohol sensitivity. Clinical studies show a disproportion of POMC cleavage products in the CSF of chronic alcoholics (reduced beta-endorphin versus increased ACTH contents), together with remarkable indications for baseline differences in beta-endorphin levels. Errors within the genetic sequence of POMC are suggested to underlie alcohol-seeking behavior.
Topics: Alcoholism; Animals; Ethanol; Humans; Pro-Opiomelanocortin; Protein Processing, Post-Translational; RNA, Messenger; beta-Endorphin
PubMed: 2969250
DOI: 10.1016/0741-8329(88)90014-6 -
Current Drug Targets Nov 2009Long known for its anti-nociceptive effects, the opioid beta-endorphin is also reported to have rewarding and reinforcing properties and to be involved in stress... (Review)
Review
Long known for its anti-nociceptive effects, the opioid beta-endorphin is also reported to have rewarding and reinforcing properties and to be involved in stress response. In this manuscript we summarize the present neurobiological and behavioral evidence regarding the role of beta-endorphin in stress-related psychiatric disorders, depression and PTSD. There is existing data that support the importance of beta-endorphin neurotransmission in mediating depression. As for PTSD, however, the data is thus far circumstantial. The studies described herein used diverse techniques, such as biochemical measurements of beta-endorphin in various brain sites and behavioral monitoring, in two animal models of depression and PTSD. We suggest that the pathways for stress-related psychiatric disorders, depression and PTSD, converge to a common pathway in which beta-endorphin is a modulating element of distress. This may occur via its interaction with the mesolimbic monoaminergic system and also by its interesting effects on learning and memory. The possible involvement of beta-endorphin in the process of stress-related psychiatric disorders, depression and PTSD, is discussed.
Topics: Animals; Disease Models, Animal; Memory; Rats; Rats, Sprague-Dawley; Stress Disorders, Post-Traumatic; beta-Endorphin
PubMed: 19702553
DOI: 10.2174/138945009789735147