Journal articles: 'Endogenous opioids'

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Herz, Albert. "Opioid reward mechanisms: a key role in drug abuse?" Canadian Journal of Physiology and Pharmacology 76, no. 3 (1998): 252–58. http://dx.doi.org/10.1139/y98-017.

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There is increasing evidence to implicate the mesolimbic dopamine system in the rewarding effects of drugs of abuse such as opioids, psychostimulants, and alcohol, and in addition endogenous opioids may play a key role in the underlying adaptive mechanisms. Opioid agonists with affinity for µ and delta opioid receptors are rewarding, whereas opioid agonists with affinity for kappa receptors are aversive. These opposing motivational effects are paralleled by an increase and decrease, respectively, of dopamine release in the nucleus accumbens. Opposite effects are induced in response to selective antagonists for these different receptor types, pointing to tonically active endogenous opioid reward mechanisms. Withdrawal from chronic morphine results in sensitization for opioid reward; an effect that is counteracted by kappa opioid agonists. The rewarding effects of psychostimulants such as cocaine and amphetamine, mediated by the mesolimbic dopamine pathway, are modulated by opioid mechanisms in both directions: sensitization by morphine pretreatment, inhibition by kappa receptor agonists. A modulatory role of endogenous opioids is also suggested from biochemical data, showing increased dynorphin and kappa receptor expression after chronic cocaine treatment. Alcohol reward involves the mesolimbic reward system also, and opioids modulate this behaviour. Naltrexone as well as selective µ and delta opioid receptor antagonists decrease alcohol consumption in operant conditioning models. Biochemical approaches point to a functional deficit of endogenous opioids in genetic models exhibiting high prevalence for alcohol intake. The therapeutic implications of these data are discussed.Key words: reward mechanisms, endogenouos opioid systems, psychostimulants, alcohol.

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Smith, Howard. "Peripherally-Acting Opioids." Pain Physician 2s;11, no. 3;2s (2008): S121—S132. http://dx.doi.org/10.36076/ppj.2008/11/s121.

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Opioids are broad-spectrum analgesics with potent pain-relieving qualities but also with potential adverse effects related to both short-term and long-term therapy. Researchers have attempted to alter existing opioid analgesics, utilize different routes/ formulations, or combine opioid analgesics with other compounds in efforts to improve analgesia while minimizing adverse effects. Exogenous opioids, administered in efforts to achieve analgesia, work by mimicking the actions of endogenous opioids. Endogenous opioids and their receptors are located in the brain (supraspinal areas), spinal cord, and periphery. Although opioids and opioid receptors in the brain and spinal cord have received much attention over many years, peripheral endogenous opioid analgesic systems have only been extensively studied during the past decade. It has been known since 1990 that following injection into the rodent hindpaw, d-Ala2 , N-Me-Phe4 , Gly5 -ol-enkephalin (DAMGO) [a muopioid receptor agonist] probably exerts its antinociceptive effects locally, since the doses administered are too low to have an effect in the central nervous system (CNS). This notion has been supported by the observation that the quaternary compound morphine methyliodide, which does not as readily cross the bloodbrain barrier and enter the CNS, produced antinociception following intradermal administration into the hindpaw, but not when the same dose was administered systemically (subcutaneously at a distant site). With a growing appreciation of peripheral endogenous opioids, peripheral endogenous opioid receptors, and peripheral endogenous opioid analgesic systems, investigators began growing hopeful that it may be possible to achieve adequate analgesics while avoiding unwanted central untoward adverse effects (e.g. respiratory depression, somnolence, addiction). Peripherally-acting opioids, which capitalize on peripheral endogenous opioid analgesic systems, may be one potential future strategy which may be utilized in efforts to achieve potent analgesia with minimal side effects. Key words: Pain, opioids, immune cells, peripherally-acting opioids (PAO), leukocytes, inflammatory pain, peripheral analgesia

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Bovill, James G. "Endogenous opioids and opioid receptors." Current Opinion in Anaesthesiology 6, no. 4 (1993): 668–72. http://dx.doi.org/10.1097/00001503-199308000-00014.

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Corder, Gregory, Daniel C. Castro, Michael R. Bruchas, and Grégory Scherrer. "Endogenous and Exogenous Opioids in Pain." Annual Review of Neuroscience 41, no. 1 (2018): 453–73. http://dx.doi.org/10.1146/annurev-neuro-080317-061522.

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Opioids are the most commonly used and effective analgesic treatments for severe pain, but they have recently come under scrutiny owing to epidemic levels of abuse and overdose. These compounds act on the endogenous opioid system, which comprises four G protein–coupled receptors (mu, delta, kappa, and nociceptin) and four major peptide families (β-endorphin, enkephalins, dynorphins, and nociceptin/orphanin FQ). In this review, we first describe the functional organization and pharmacology of the endogenous opioid system. We then summarize current knowledge on the signaling mechanisms by which opioids regulate neuronal function and neurotransmission. Finally, we discuss the loci of opioid analgesic action along peripheral and central pain pathways, emphasizing the pain-relieving properties of opioids against the affective dimension of the pain experience.

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Santiago, T. V., and N. H. Edelman. "Opioids and breathing." Journal of Applied Physiology 59, no. 6 (1985): 1675–85. http://dx.doi.org/10.1152/jappl.1985.59.6.1675.

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This review summarizes recent developments on the effects of opiate drugs and the various endogenous opioid peptides on breathing. These developments include demonstration of receptors and site-specific effects of application of opioids in the pons and medulla, demonstration of variable tolerance of respiratory responses in addicted individuals as well as their offspring, and demonstration of an endogenous opioid influence on breathing in early neonatal life and in certain physiological settings and disease states. The validity and limitations of using naloxone as a tool to uncover postulated endogenous opioid influences are also discussed as well as the potential problems imposed by the various settings in which this opiate antagonist drug is used. It is concluded that some parallelism exists between the role of endogenous opioids in pain modulation and their role in respiration especially in adults. Although more studies are needed especially with regard to defining specific effects of the various opioid receptors and ligands, it is felt that the effects of endogenous opioids on the control of breathing will probably be one of modulating the responses to drugs or nociceptive respiratory stimuli through inhibitory pathways.

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Rees, John M. H. "Endogenous opioids." Baillière's Clinical Rheumatology 1, no. 1 (1987): 27–56. http://dx.doi.org/10.1016/s0950-3579(87)80028-6.

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Gintzler, PhD, Alan R., and Nai-Jiang Liu, MD, PhD. "Harnessing endogenous opioids for pain relief: Fantasy vs reality." Journal of Opioid Management 16, no. 1 (2020): 67–72. http://dx.doi.org/10.5055/jom.2020.0552.

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Objective: To review evidence demonstrating efficacy and feasibility of harnessing the activity of endogenous opioid analgesic systems for pain management.Methods: The authors sought to summarize a wealth of data that establish proof of concept that the analgesic activity of endogenous opioids can be exploited to clinically benefit from the enormous pain-relieving abilities of these peptides without contributing to the current crisis of death by synthetic opioid overdose.Results: There is a plethora of studies demonstrating that not only can endogenous opioids mediate placebo-induced antinociception but they are also active in modulating clinical pain. Earlier studies convincingly demonstrate the effectiveness of psychological strategies to coopt endogenous opioid analgesic systems to produce pain relief. The challenge is to define pharmacological targets for activating endogenous opioid analgesia reliably in a clinical setting. Based on insights gleaned from mechanisms underlying the ebb and flow of analgesic responsiveness to the spinal application of endomorphin 2, multiple signaling proteins were identified that activate endogenous spinal opioid analgesia. Notably, this was achieved in the absence of any exogenous synthetic opioid.Conclusions: Utilization of drugs that harness endogenous opioid antinociception in accordance with varying physiological states represents a novel approach for effective pain management while mitigating the present epidemic of death by synthetic opioid overdose.

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Liren, A.-L., and G. Feuerstein. "The Opioid System in Circulatory Control." Physiology 7, no. 1 (1992): 26–30. http://dx.doi.org/10.1152/physiologyonline.1992.7.1.26.

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Opioid peptides and multiple opioid receptors are found in brain cardiovascular nuclei, autonomic ganglia, the heart, and blood vessels, and opioids induce potent cardiovascular changes. The role of endogenous opioids in normal cardiovascular homeostasis is unclear;however, current data suggest opioid involvement in stress.

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Ismail, Zahinoor, and Nady el-Guebaly. "Nicotine and Endogenous Opioids: Toward Specific Pharmacotherapy." Canadian Journal of Psychiatry 43, no. 1 (1998): 37–42. http://dx.doi.org/10.1177/070674379804300103.

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Objective: To address the theoretical framework behind opioid receptor antagonism for the treatment of nicotine abuse. The current literature is reviewed with a focus on opioid–nicotine interactions in animals and humans. Furthermore, previous studies addressing the effect of opioid antagonism on smoking behaviour are reviewed critically with a focus on suggestions and implications for future trials. Method: Computerized data bases and reference lists of existing articles were searched for prior publications in 3 areas: 1) the association between nicotine and endogenous opioids, 2) nicotine and reward, and 3) opioid antagonism in the treatment of nicotine use. Results: Nicotine affects the mesolimbic reward pathway postsynaptically via nicotinic cholinergic receptors and presynaptically via the central nervous system's (CNS) neurohumoral pathways. Thus nicotine results in the release of endogenous opioids that bind to μ receptors, which increases the release of dopamine along this pathway. Studies to date have shown mixed results on the effect of opioid antagonism on smoking behaviour. Conclusions: The role of opioid antagonism on smoking behaviour is unclear, despite the publication of 5 trials on the subject. Further trials of longer duration should be undertaken and use both longer-acting medications and those more specific to the μ receptor to further focus on the rewarding aspects of nicotine ingestion, thus addressing the craving for this drug. The development of adequate compounds has just begun, and psychiatrists can hope to have a more specific pharmacotherapy to address the cravings and short-term rewards of nicotine use.

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Meier, Isabell M., Marie Eikemo, and Siri Leknes. "The Role of Mu-Opioids for Reward and Threat Processing in Humans: Bridging the Gap from Preclinical to Clinical Opioid Drug Studies." Current Addiction Reports 8, no. 2 (2021): 306–18. http://dx.doi.org/10.1007/s40429-021-00366-8.

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Abstract Purpose of Review Opioid receptors are widely expressed in the human brain. A number of features commonly associated with drug use disorder, such as difficulties in emotional learning, emotion regulation and anhedonia, have been linked to endogenous opioid signalling. Whereas chronic substance use and misuse are thought to alter the function of the mu-opioid system, the specific mechanisms are not well understood. We argue that understanding exogenous and endogenous opioid effects in the healthy human brain is an essential foundation for bridging preclinical and clinical findings related to opioid misuse. Here, we will examine psychopharmacological evidence to outline the role of the mu-opioid receptor (MOR) system in the processing of threat and reward, and discuss how disruption of these processes by chronic opioid use might alter emotional learning and reward responsiveness. Recent Findings In healthy people, studies using opioid antagonist drugs indicate that the brain’s endogenous opioids downregulate fear reactivity and upregulate learning from safety. At the same time, endogenous opioids increase the liking of and motivation to engage with high reward value cues. Studies of acute opioid agonist effects indicate that with non-sedative doses, drugs such as morphine and buprenorphine can mimic endogenous opioid effects on liking and wanting. Disruption of endogenous opioid signalling due to prolonged opioid exposure is associated with some degree of anhedonia to non-drug rewards; however, new results leave open the possibility that this is not directly opioid-mediated. Summary The available human psychopharmacological evidence indicates that the healthy mu-opioid system contributes to the regulation of reward and threat processing. Overall, endogenous opioids can subtly increase liking and wanting responses to a wide variety of rewards, from sweet tastes to feelings of being connected to close others. For threat-related processing, human evidence suggests that endogenous opioids inhibit fear conditioning and reduce the sensitivity to aversive stimuli, although inconsistencies remain. The size of effects reported in healthy humans are however modest, clearly indicating that MORs play out their role in close concert with other neurotransmitter systems. Relevant candidate systems for future research include dopamine, serotonin and endocannabinoid signalling. Nevertheless, it is possible that endogenous opioid fine-tuning of reward and threat processing, when unbalanced by e.g. opioid misuse, could over time develop into symptoms associated with opioid use disorder, such as anhedonia and depression/anxiety.

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Randhawa, Puneet Kaur, and Amteshwar Singh Jaggi. "Opioids in Remote Ischemic Preconditioning-Induced Cardioprotection." Journal of Cardiovascular Pharmacology and Therapeutics 22, no. 2 (2016): 112–21. http://dx.doi.org/10.1177/1074248416660621.

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Remote ischemic preconditioning (RIPC) is an intriguing process whereby transient regional ischemia and reperfusion episodes to remote tissues including skeletal, renal, mesenteric provide protection to the heart against sustained ischemia–reperfusion-induced injury. Clinically, this technique has been used in patients undergoing various surgical interventions including coronary artery bypass graft surgery, abdominal aortic aneurysm repair, percutaneous coronary intervention, and heart valve surgery. The endogenous opioid system is extensively expressed in the brain to modulate pain sensation. Besides the role of opioids in relieving pain, numerous researchers have found their critical involvement in evoking cardioprotective effects. Endogenous opioids including endorphins, enkephalins, and dynorphins are released during RIPC and are critically involved in mediating RIPC-induced cardioprotective effects. It has been suggested that during RIPC, the endogenous opioids may be released into the systemic circulation and may travel via bloodstream that act on the myocardial opioid receptors to induce cardioprotection. The present review describes the potential role of opioids in mediating RIPC-induced cardioprotection.

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Petrocelli, Giovannamaria, Luca Pampanella, Provvidenza M. Abruzzo, Carlo Ventura, Silvia Canaider, and Federica Facchin. "Endogenous Opioids and Their Role in Stem Cell Biology and Tissue Rescue." International Journal of Molecular Sciences 23, no. 7 (2022): 3819. http://dx.doi.org/10.3390/ijms23073819.

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Opioids are considered the oldest drugs known by humans and have been used for sedation and pain relief for several centuries. Nowadays, endogenous opioid peptides are divided into four families: enkephalins, dynorphins, endorphins, and nociceptin/orphanin FQ. They exert their action through the opioid receptors (ORs), transmembrane proteins belonging to the super-family of G-protein-coupled receptors, and are expressed throughout the body; the receptors are the δ opioid receptor (DOR), μ opioid receptor (MOR), κ opioid receptor (KOR), and nociceptin/orphanin FQ receptor (NOP). Endogenous opioids are mainly studied in the central nervous system (CNS), but their role has been investigated in other organs, both in physiological and in pathological conditions. Here, we revise their role in stem cell (SC) biology, since these cells are a subject of great scientific interest due to their peculiar features and their involvement in cell-based therapies in regenerative medicine. In particular, we focus on endogenous opioids’ ability to modulate SC proliferation, stress response (to oxidative stress, starvation, or damage following ischemia–reperfusion), and differentiation towards different lineages, such as neurogenesis, vasculogenesis, and cardiogenesis.

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Gibula-Tarlowska, Ewa, and Jolanta H. Kotlinska. "Crosstalk between Opioid and Anti-Opioid Systems: An Overview and Its Possible Therapeutic Significance." Biomolecules 10, no. 10 (2020): 1376. http://dx.doi.org/10.3390/biom10101376.

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Opioid peptides and receptors are broadly expressed throughout peripheral and central nervous systems and have been the subject of intense long-term investigations. Such studies indicate that some endogenous neuropeptides, called anti-opioids, participate in a homeostatic system that tends to reduce the effects of endogenous and exogenous opioids. Anti-opioid properties have been attributed to various peptides, including melanocyte inhibiting factor (MIF)-related peptides, cholecystokinin (CCK), nociceptin/orphanin FQ (N/OFQ), and neuropeptide FF (NPFF). These peptides counteract some of the acute effects of opioids, and therefore, they are involved in the development of opioid tolerance and addiction. In this work, the anti-opioid profile of endogenous peptides was described, mainly taking into account their inhibitory influence on opioid-induced effects. However, the anti-opioid peptides demonstrated complex properties and could show opioid-like as well as anti-opioid effects. The aim of this review is to detail the phenomenon of crosstalk taking place between opioid and anti-opioid systems at the in vivo pharmacological level and to propose a cellular and molecular basis for these interactions. A better knowledge of these mechanisms has potential therapeutic interest for the control of opioid functions, notably for alleviating pain and/or for the treatment of opioid abuse.

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Imura, H., Y. Kato, Y. Nakai, et al. "Endogenous opioids and related peptides: from molecular biology to clinical medicine The Sir Henry Dale Lecture for 1985." Journal of Endocrinology 107, no. 2 (1985): 147–57. http://dx.doi.org/10.1677/joe.0.1070147.

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ABSTRACT Advances in techniques in molecular biology have facilitated the research into endogenous opioids and related peptides in several ways. The organization and expression of genes and the primary structure of three precursor proteins of opioid peptides have been elucidated. These studies predicted the presence of potentially bioactive peptides, which has been confirmed by later studies. Advances in techniques in protein chemistry have helped to elucidate the distribution and molecular forms of endogenous opioids and related peptides in the body, and the processing of precursor proteins. Studies on the function of these peptides have shown a broad spectrum of actions. Leumorphin, a newly identified peptide, has been shown to exhibit unique biological activities. In spite of extensive studies, the physiological and pathophysiological significance of opioid peptide systems are not yet completely understood. This is mainly due to the paucity of our knowledge about opioid receptors. Further studies on the subtypes of opioid receptors will help to elucidate all aspects of the function of endogenous opioids and related peptides. J. Endocr. (1985) 107, 147–157

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García-López, Celia, Carmen Gómez-Huertas, José-María Sánchez-González, et al. "Opioids and Ocular Surface Pathology: A Literature Review of New Treatments Horizons." Journal of Clinical Medicine 11, no. 5 (2022): 1424. http://dx.doi.org/10.3390/jcm11051424.

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This review discusses the role of opioids in the corneal surface and the different pathways and therapeutic methods of management. A literature review was performed using PubMed database. For the database search, the main searching words “opioid” and “topical opioid treatment” were used with the descriptors “cornea”, “ocular surface”, “neuropathic corneal pain”, “corneal sensitivity” and “naltrexone”; original scientific articles and reviews were included to achieve the purpose of the review. The endogenous opioid system has relevant functions in the organism, and in daily use, opioids are used as painkillers. However, these drugs may be employed for other indications as opioid pathways have a wide spectrum. The corneal surface for topical treatment is easily accessible, hence sparing the side effects of systemic opioids. Instillation of opioid antagonist substances, such as naltrexone, increases corneal healing rates and stimulates the division of corneal epithelium cells without deleterious effects. The natural modulation of endogenous opioids controls different forms of pain, including inflammatory and neuropathic pain, both in the ocular surface and in the central nervous system. There are diverse methods in controlling pain using opioids, especially in refractory forms. This review attempts to collect the literature about corneal surface and opioid pathways to provide an overview image and a possible direction of the news treatments.

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Weinberger, S. E., R. A. Steinbrook, D. B. Carr, et al. "Endogenous opioids and ventilatory responses to hypercapnia in normal humans." Journal of Applied Physiology 58, no. 5 (1985): 1415–20. http://dx.doi.org/10.1152/jappl.1985.58.5.1415.

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Though administration of opioid peptides depresses ventilation and ventilatory responsiveness, the role of endogenous opioid peptides in modulating ventilatory responsiveness is not clear. We studied the interaction of endogenous opioids and ventilatory responses in 12 adult male volunteers by relating hypercapnic responsiveness to plasma levels of immunoactive beta-endorphin and by administering the opiate antagonist naloxone. Ventilatory responsiveness to hypercapnia was not altered by pretreatment with naloxone, and this by itself suggests that endogenous opioids have no role in modulating this response. However, there was an inverse relationship between basal levels of immunoactive beta-endorphin in plasma and ventilatory responsiveness to CO2. Furthermore, plasma beta-endorphin levels rose after short-term hypercapnia but only when subjects had been pretreated with naloxone. We conclude that measurement of plasma endorphin levels suggests relationships between endogenous opioid peptides and ventilatory responses to CO2 that are not apparent in studies limited to assessing the effect of naloxone.

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Davis, Mellar. "Cholestasis and Endogenous Opioids." Clinical Pharmacokinetics 46, no. 10 (2007): 825–50. http://dx.doi.org/10.2165/00003088-200746100-00002.

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Van Ree, Jan M., Raymond J. M. Niesink, Leo Van Wolfswinkel, et al. "Endogenous opioids and reward." European Journal of Pharmacology 405, no. 1-3 (2000): 89–101. http://dx.doi.org/10.1016/s0014-2999(00)00544-6.

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Cooper, Steven J. "Palatability and endogenous opioids." Regulatory Peptides 54, no. 1 (1994): 67–68. http://dx.doi.org/10.1016/0167-0115(94)90392-1.

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Kościelniak-Merak, Barbara, Ilona Batko, Krzysztof Kobylarz, Krystyna Sztefko, Magdalena Kocot-Kępska, and Przemysław J. Tomasik. "Impact of Intravenous, Perioperative-Administrated Lidocaine on Postoperative Serum Levels of Endogenous Opioids in Children." Current Pharmaceutical Design 25, no. 30 (2019): 3209–15. http://dx.doi.org/10.2174/1381612825666190718153209.

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Background: Endogenous opioids are neuropeptides involved in pain-relieving processes. In the periphery, they are synthesised and stored in cells of the immune system. Objective: In the current study, we describe the influence of perioperative, intravenous (i.v.) lidocaine infusion in children on postoperative, serum endogenous opioid concentrations in children. Methods: Forty-four children undergoing major spinal surgery were enrolled in the cohort study. They were divided into two groups: group A (n = 21) generally anesthetised with fentanyl, propofol, rocuronium, a mixture of oxygen/air/sevoflurane and with analgetics and co-analgetics: morphine, acetaminophen, metamizole, gabapentin, dexamethason and group B (n = 23) where, in addition to the above-described general anesthesia, patients were given i.v. lidocaine as a co-analgesic. We also recruited 20 healthy age- and gender-matched children (group C). We measured endogenous opioid levels in serum using immunoenzymatic methods. We evaluated postoperative pain intensity using a numerical or visual pain scale and demand for morphine. Results: The levels of measured endogenous opioids were similar in the control and in the studied groups before surgery. We noted that group B patients had lower pain intensity when compared to group A subjects. In group B, the elevated serum concentrations of β -endorphin, enkephalin and dynorphin in the postoperative period were reported. We also observed that the levels of endogenous opioids negatively correlated with morphine requirements and positively correlated with lidocaine concentration. Conclusion: Multidrug pain management including lidocaine seems to be more efficient than models without lidocaine. The endogenous opioid system should be considered as a novel target for pain relief therapy in children.

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Kapusta, D. R., and J. C. Obih. "Role of endogenous central opioid mechanisms in maintenance of body sodium balance." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 3 (1995): R723—R730. http://dx.doi.org/10.1152/ajpregu.1995.268.3.r723.

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The role of endogenous central opioids in the regulation of renal function was studied in Sprague-Dawley rats. In metabolism studies, changes in sodium balance were examined during normal dietary sodium intake (days 1-7; Na+ of 174 meq/kg) and sodium restriction (days 8-14; Na+ of 4.0 meq/kg). The influence of endogenous central opioids was investigated by repeating the protocol in the same rats during intracerebroventricular infusion of the opioid antagonist naltrexone methylbromide (NMBR). Intracerebroventricular NMBR did not alter sodium balance in rats fed normal sodium chow. In contrast, on low-sodium days 8 and 9, rats exhibited a more negative sodium balance during intracerebroventricular NMBR (day 8; -1,191 +/- 37 mu eq) compared with respective predrug control levels (day 8; -641 +/- 39 mu eq). Subcutaneous NMBR did not alter renal adaptation to sodium restriction. Thus central opioids are not involved in the maintenance of sodium balance during normal sodium intake. However, when dietary sodium is restricted, central opioid pathways are activated as a mechanism to maximally retain sodium.

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Lipkowski, A. W., A. Misicka, D. B. Carr, G. Ronsisvalle, Dariusz Kosson, and I. Maszczynska Bonney. "Neuropeptide mimetics for pain management." Pure and Applied Chemistry 76, no. 5 (2004): 941–50. http://dx.doi.org/10.1351/pac200476050941.

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The discovery of numerous endogenous neuropeptides that participate in the formation, transmission, modulation, and perception of pain signals offers numerous strategies for the development of new analgesics. Nevertheless, the same research has not yet replaced opioids as the gold standard of pain treatment. Therefore, one possible avenue of drug development may shift interest from searching for receptor-selective opioids to creating an arsenal of drugs that target multiple opioid and non-opioid sites simultaneously. The presented short review focuses on the development of potential analgesic peptidomimetic compounds based upon opioid neuropeptides and substance P.

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O'Brien, Charles P., Lars Y. Terenius, Fred Nyberg, A. T. McLellan, and Ingrid Eriksson. "Endogenous opioids in cerebrospinal fluid of opioid-dependent humans." Biological Psychiatry 24, no. 6 (1988): 649–62. http://dx.doi.org/10.1016/0006-3223(88)90139-4.

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Stagg, Nicola J., Heriberto P. Mata, Mohab M. Ibrahim, et al. "Regular Exercise Reverses Sensory Hypersensitivity in a Rat Neuropathic Pain Model." Anesthesiology 114, no. 4 (2011): 940–48. http://dx.doi.org/10.1097/aln.0b013e318210f880.

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Background Exercise is often prescribed as a therapy for chronic pain. Short-term exercise briefly increases the production of endogenous analgesics, leading to transient antinociception. In limited studies, exercise produced sustained increases in endogenous opioids, sustained analgesia, or diminished measures of chronic pain. This study tests the hypothesis that regular aerobic exercise leads to sustained reversal of neuropathic pain by activating endogenous opioid-mediated pain modulatory systems. Methods After baseline measurements, the L5 and L6 spinal nerves of male Sprague-Dawley rats were tightly ligated. Animals were randomized to sedentary or 5-week treadmill exercise-trained groups. Thermal and tactile sensitivities were assessed 23 h after exercise, using paw withdrawal thresholds to von Frey filaments and withdrawal latencies to noxious heat. Opioid receptor antagonists were administered by subcutaneous, intrathecal, or intracerebroventricular injection. Opioid peptides were quantified using immunohistochemistry with densitometry. Results Exercise training ameliorated thermal and tactile hypersensitivity in spinal nerve-ligated animals within 3 weeks. Sensory hypersensitivity returned 5 days after discontinuation of exercise training. The effects of exercise were reversed by using systemically or intracerebroventricularly administered opioid receptor antagonists and prevented by continuous infusion of naltrexone. Exercise increased β-endorphin and met-enkephalin content in the rostral ventromedial medulla and the mid-brain periaqueductal gray area. Conclusions Regular moderate aerobic exercise reversed signs of neuropathic pain and increased endogenous opioid content in brainstem regions important in pain modulation. Exercise effects were reversed by opioid receptor antagonists. These results suggest that exercise-induced reversal of neuropathic pain results from an up-regulation of endogenous opioids.

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Lishmanov, Yu B., L. N. Maslov, N. Yu Naryzhnaya, et al. "ENDOGENOUS OPIOID SYSTEM AS A MEDIATOR OF ACUTE AND LONG-TERM ADAPTATION TO STRESS. PROSPECTS FOR CLINICAL USE OF OPIOID PEPTIDES." Annals of the Russian academy of medical sciences 67, no. 6 (2012): 73–82. http://dx.doi.org/10.15690/vramn.v67i6.287.

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It has been well established that opioid peptides (OPs) affect various hormonal systems. Opioids exhibit stress-limiting and gastro-protective effects in stressed animals, acting via μ- and δ-opioid receptors (OR). Peripheral μ-OR stimulation by endogenous and exogenous opioids increases cardiac tolerance to pathological consequences of stress. Enhancement of prostacyclin synthesis, decrease of thromboxane production as well as suppression of lipid peroxidation can be directly responsible for cardioprotective effects of OPs in stressed animals. Adaptive responses are accompanied by increased OP levels in blood and tissues. Reduction of ventricular arrhythmias induced by repeated short-term immobilization stress is mediated via μ-OR stimulation by endogenous opioids, while δ-OR account for an antiarrhythmic effect of adaptation to chronic intermittent hypobaric hypoxia. The mechanism of infarct size-limiting effect of continuous normobaric hypoxia involves both μ- and δ-OR stimulation. Peptide OR agonists can be considered in future clinical practice for treatment of withdrawal syndrome, stress-related cardiac disease or myocardial injury caused by ischemia-reperfusion insult.

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Mani, Ali R., Reza Rasool, Sara Montagnese, and Ahmad R. Dehpour. "Endogenous opioids and liver disease." Scandinavian Journal of Gastroenterology 41, no. 1 (2006): 1–11. http://dx.doi.org/10.1080/00365520500287533.

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Howman, Sonia F., and Jeffrey S. Groeger. "Endogenous opioids and hypoxic survival." Critical Care Medicine 27, no. 9 (1999): 2057–58. http://dx.doi.org/10.1097/00003246-199909000-00073.

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HOLADAY, JOHN W., FRANK C. TORTELLA, JOSEPH B. LONG, G. L. BELENKY, and ROBERT J. HITZEMANN. "Endogenous Opioids and Their Receptors." Annals of the New York Academy of Sciences 462, no. 1 Electroconvul (1986): 124–39. http://dx.doi.org/10.1111/j.1749-6632.1986.tb51247.x.

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Gerrits, M. A. F. M., and J. M. van Ree. "Endogenous opioids and drug dependence." European Neuropsychopharmacology 13 (March 2003): S4—S5. http://dx.doi.org/10.1016/s0924-977x(03)90002-2.

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Shoupe, Donna, and Rogerio Lobo. "Endogenous Opioids in the Menopause." Seminars in Reproductive Medicine 5, no. 02 (1987): 199–206. http://dx.doi.org/10.1055/s-2008-1033673.

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Zagon, Ian S., and Patricia J. McLaughlin. "Endogenous opioids and brain development." International Journal of Developmental Neuroscience 3, no. 4 (1985): 425. http://dx.doi.org/10.1016/0736-5748(85)90103-0.

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Džoljić, E. D. "Central effects of endogenous opioids." European Journal of Pharmacology 183, no. 6 (1990): 2315. http://dx.doi.org/10.1016/0014-2999(90)93870-v.

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Van Ree, J. M., and M. A. F. M. Gerrits. "Endogenous opioids and experimental addiction." European Neuropsychopharmacology 6 (June 1996): 163. http://dx.doi.org/10.1016/0924-977x(96)88061-8.

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34

Panksepp, J., M. Leboyer, M. Bovard, JM Launay, and P. Lensing. "Endogenous opioids and childhood autism." Regulatory Peptides 53 (February 1994): S169—S170. http://dx.doi.org/10.1016/0167-0115(94)90294-1.

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35

Piccoli, Renata, Dominique Melck, Antonietta Spagnuolo, Stefania Vescia, and Laura Zanetti. "Endogenous opioids in marine invertebrates." Comparative Biochemistry and Physiology Part C: Comparative Pharmacology 80, no. 2 (1985): 237–40. http://dx.doi.org/10.1016/0742-8413(85)90048-9.

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Comer, C. R., J. S. Grunstein, R. J. Mason, S. C. Johnston, and M. M. Grunstein. "Endogenous opioids modulate fetal rabbit lung maturation." Journal of Applied Physiology 62, no. 6 (1987): 2141–46. http://dx.doi.org/10.1152/jappl.1987.62.6.2141.

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To test the hypothesis that endogenous opioids modulate fetal lung development, separate groups of pregnant rabbits received daily injections of saline, morphine (1 mg/kg body wt), or the opioid antagonist naloxone (0.4 and 5.0 mg) for 10 days during their last trimester of pregnancy. The corresponding groups of fetuses were then delivered prematurely on day 28 of gestation (term approximately 31 days) and evaluated with respect to differences in body weight, lung weight, and the ratios of wet to dry lung weight and lung dry weight to body weight, the static inflation and deflation air and saline pressure-volume (P-V) characteristics of the lungs, and lung morphology. Mean values for body weight, lung weight, and the ratios of lung wet to dry weight and lung dry weight to body weight were not significantly different among the saline control (C), morphine (M)-, and naloxone (NLX)-treated fetuses. On the other hand, the fetal air P-V curves varied significantly (P less than 0.001), wherein the M-treated group depicted increased lung distensibility and alveolar stability on lung deflation, whereas the opposite was obtained in the NLX-treated fetuses. Moreover, morphometric analyses demonstrated that the mean alveolar air space-to-tissue ratio in lungs from M-treated fetuses were significantly greater than that observed either in C or in NLX-treated fetuses (P less than 0.05); however, the air space-to-tissue ratio did not significantly vary between the C and NLX-treated animals. These observations provide new evidence that endogenous opioids enhance fetal lung maturation.

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Kunecki, Marcin, Wojciech Płazak, Piotr Podolec, and Krzysztof S. Gołba. "Effects of endogenous cardioprotective mechanisms on ischemia-reperfusion injury." Postępy Higieny i Medycyny Doświadczalnej 71 (January 10, 2017): 20–31. http://dx.doi.org/10.5604/01.3001.0010.3786.

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Ischemic heart disease have been remarked as a leading cause of morbidity and mortality in adults. Early restoration of cardiac perfusion is necessary to restore perfusion of ischemic heart muscle. Effective revascularization reduce mortality by limiting myocardial necrosis at the acute phase of the cardiac infarction. However, reperfusion may induce a cascade of pathophysiological reactions causing the increase of the infarct area of the myocardium This phenomenon known as ischemia-reperfusion injury is responsible for up to 50% of the final infarct size. Sequences of brief episodes of nonlethal ischemia and reperfusion applied before (preconditioning — IPC) or after (postconditioning — POC) the coronary occlusion are well documented to reduce the ischemiareperfusion injury. These phenomena improve cardiac function by mobilizing the molecular and cellular mechanisms limiting reperfusion injury. The mechanisms underlying IPC or POC are still not clarified, but strong experimental evidence suggests that opioids may be the part of the endogenous cardioprotective response to I/R injury. Stimulation of opioid receptors activates related to POC mechanisms affecting protection to the ischemic myocardium, while the use of non-selective opioid receptor antagonist - naloxone reduces this effect. There is no consensus that the subtype of opioid receptor is responsible for the protection of the human heart muscle.Morphine may reduce cardiac preload by peripheral vasodilatation. Numerous studies show a direct cardioprotective effect of the opioid pathway in ischemic conditions. Opioids act via membrane receptors: μ, δ, κ. The predominant subtype in the human cardiac cells are μ- and δ – opioid receptors. It has been hypothetized that opioid receptor activation exerts cardioprotection in human heart muscle pathway what may give insight into the explanation of the protective mechanisms in the acute myocardial infarction.

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Appleyard, Suzanne M., Michael Hayward, Juan I. Young та ін. "A Role for the Endogenous Opioid β-Endorphin in Energy Homeostasis". Endocrinology 144, № 5 (2003): 1753–60. http://dx.doi.org/10.1210/en.2002-221096.

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Proopiomelanocortin (POMC) neurons in the hypothalamus are direct targets of the adipostatic hormone leptin and contribute to energy homeostasis by integrating peripheral and central information. The melanocortin and β-endorphin neuropeptides are processed from POMC and putatively coreleased at axon terminals. Melanocortins have been shown by a combination of pharmacological and genetic methods to have inhibitory effects on appetite and body weight. In contrast, pharmacological studies have generally indicated that opioids stimulate food intake. Here we report that male mice engineered to selectively lack β-endorphin, but that retained normal melanocortin signaling, were hyperphagic and obese. Furthermore, β-endorphin mutant and wild-type mice had identical orexigenic responses to exogenous opioids and identical anorectic responses to the nonselective opioid antagonist naloxone, implicating an alternative endogenous opioid tone to β-endorphin that physiologically stimulates feeding. These genetic data indicate that β-endorphin is required for normal regulation of feeding, but, in contrast to earlier reports suggesting opposing actions of β-endorphin and melanocortins on appetite, our results suggest a more complementary interaction between the endogenously released POMC-derived peptides in the regulation of energy homeostasis.

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Telford, G. L., R. E. Condon, and J. H. Szurszewski. "Opioid receptors and the initiation of migrating myoelectric complexes in dogs." American Journal of Physiology-Gastrointestinal and Liver Physiology 256, no. 1 (1989): G72—G77. http://dx.doi.org/10.1152/ajpgi.1989.256.1.g72.

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The role of endogenous opioids and opioid receptors in the control of migrating myoelectric complexes (MMCs) was studied in conscious dogs implanted with silver-silver chloride electrodes. In normal fasted dogs, MMC cycle times were 103 +/- 7 min in the duodenum. During naloxone infusion (1-2 mg/kg iv, then 0.2-1.0 mg.kg-1.h-1 iv) cycle times increased to 219 +/- 29 min (P less than 0.01). Naloxone (2 mg/kg iv, then 1 mg.kg-1.h-1 iv) had no effect on the response of the small intestine to bethanecol (5 mg sc) or to feeding. Pretreatment with naloxone (2 mg/kg iv) 5 min before the administration of motilin (400-500 micrograms/kg iv) did not block the initiation of MMCs by motilin. In separate experiments, animals were pretreated with the positive or negative isomer of the opioid receptor antagonist WIN-44,441 (0.2 mg/kg iv) 5 min before morphine administration. The negative isomer binds to opioid receptors whereas the positive isomer does not. The negative but not the positive isomer antagonized all effects of morphine on intestinal myoelectric activity. These studies suggest that endogenous opioids and opioid receptors may play a role in control of the initiation of MMCs and that motilin and exogenous opioids act via different mechanisms to initiate MMCs.

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Van Furth, W. R., I. G. Wolterink-Donselaar, and J. M. van Ree. "Endogenous opioids are differentially involved in appetitive and consummatory aspects of sexual behavior of male rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, no. 2 (1994): R606—R613. http://dx.doi.org/10.1152/ajpregu.1994.266.2.r606.

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The sexual activity of 40 male Wistar rats was tested weekly in a bilevel test chamber to evaluate the involvement of endogenous opioids in the appetitive and consummatory aspects of sexual behavior. It has been suggested that the increase of the anticipatory level-changing behavior over repeated testing, displayed before the introduction of a receptive female, is sexually motivated. Two doses of the opioid antagonist naloxone, 1 and 10 mg/kg, prevented the increase of the anticipatory level-changing over four repeated tests of sexually experienced rats without prior experience in the bilevel test chamber and decreased the number of level changes of rats displaying a high number of level changes. Analysis of the pattern of inhibition suggested that the lower dose of naloxone may reduce sexual reward and that, in addition, the higher dose may block the expression of motivation. In contrast, naloxone treatment facilitated the efficiency of the sexual performance, with less mounts and intromissions preceding ejaculation and a shorter ejaculation latency, implying an inhibitory role of endogenous opioids in the neural control of some aspects of sexual performance (e.g., ejaculatory threshold). These results suggest that endogenous opioids may increase sexual appetite and diminish sexual performance.

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Cleymaet, Allison M., Casey-Tyler Berezin, and Jozsef Vigh. "Endogenous Opioid Signaling in the Mouse Retina Modulates Pupillary Light Reflex." International Journal of Molecular Sciences 22, no. 2 (2021): 554. http://dx.doi.org/10.3390/ijms22020554.

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Opioid peptides and their receptors are expressed in the mammalian retina; however, little is known about how they might affect visual processing. The melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs), which mediate important non-image-forming visual processes such as the pupillary light reflex (PLR), express β-endorphin-preferring, µ-opioid receptors (MORs). The objective of the present study was to elucidate if opioids, endogenous or exogenous, modulate pupillary light reflex (PLR) via MORs expressed by ipRGCs. MOR-selective agonist [D-Ala2, MePhe4, Gly-ol5]-enkephalin (DAMGO) or antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) was administered via intravitreal injection. PLR was recorded in response to light stimuli of various intensities. DAMGO eliminated PLR evoked by light with intensities below melanopsin activation threshold but not that evoked by bright blue irradiance that activated melanopsin signaling, although in the latter case, DAMGO markedly slowed pupil constriction. CTAP or genetic ablation of MORs in ipRGCs slightly enhanced dim-light-evoked PLR but not that evoked by a bright blue stimulus. Our results suggest that endogenous opioid signaling in the retina contributes to the regulation of PLR. The slowing of bright light-evoked PLR by DAMGO is consistent with the observation that systemically applied opioids accumulate in the vitreous and that patients receiving chronic opioid treatment have slow PLR.

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Cleymaet, Allison M., Casey-Tyler Berezin, and Jozsef Vigh. "Endogenous Opioid Signaling in the Mouse Retina Modulates Pupillary Light Reflex." International Journal of Molecular Sciences 22, no. 2 (2021): 554. http://dx.doi.org/10.3390/ijms22020554.

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Opioid peptides and their receptors are expressed in the mammalian retina; however, little is known about how they might affect visual processing. The melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs), which mediate important non-image-forming visual processes such as the pupillary light reflex (PLR), express β-endorphin-preferring, µ-opioid receptors (MORs). The objective of the present study was to elucidate if opioids, endogenous or exogenous, modulate pupillary light reflex (PLR) via MORs expressed by ipRGCs. MOR-selective agonist [D-Ala2, MePhe4, Gly-ol5]-enkephalin (DAMGO) or antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) was administered via intravitreal injection. PLR was recorded in response to light stimuli of various intensities. DAMGO eliminated PLR evoked by light with intensities below melanopsin activation threshold but not that evoked by bright blue irradiance that activated melanopsin signaling, although in the latter case, DAMGO markedly slowed pupil constriction. CTAP or genetic ablation of MORs in ipRGCs slightly enhanced dim-light-evoked PLR but not that evoked by a bright blue stimulus. Our results suggest that endogenous opioid signaling in the retina contributes to the regulation of PLR. The slowing of bright light-evoked PLR by DAMGO is consistent with the observation that systemically applied opioids accumulate in the vitreous and that patients receiving chronic opioid treatment have slow PLR.

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DiCello, Jesse J., Ayame Saito, Pradeep Rajasekhar, et al. "Inflammation-associated changes in DOR expression and function in the mouse colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 315, no. 4 (2018): G544—G559. http://dx.doi.org/10.1152/ajpgi.00025.2018.

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Endogenous opioids activate opioid receptors (ORs) in the enteric nervous system to control intestinal motility and secretion. The μ-OR mediates the deleterious side effects of opioid analgesics, including constipation, respiratory depression, and addiction. Although the δ-OR (DOR) is a promising target for analgesia, the function and regulation of DOR in the colon are poorly understood. This study provides evidence that endogenous opioids activate DOR in myenteric neurons that may regulate colonic motility. The DOR agonists DADLE, deltorphin II, and SNC80 inhibited electrically evoked contractions and induced neurogenic contractions in the mouse colon. Electrical, chemical, and mechanical stimulation of the colon evoked the release of endogenous opioids, which stimulated endocytosis of DOR in the soma and proximal neurites of myenteric neurons of transgenic mice expressing DOR fused to enhanced green fluorescent protein. In contrast, DOR was not internalized in nerve fibers within the circular muscle. Administration of dextran sulfate sodium induced acute colitis, which was accompanied by DOR endocytosis and an increased density of DOR-positive nerve fibers within the circular muscle. The potency with which SNC80 inhibited neurogenic contractions was significantly enhanced in the inflamed colon. This study demonstrates that DOR-expressing neurons in the mouse colon can be activated by exogenous and endogenous opioids. Activated DOR traffics to endosomes and inhibits neurogenic motility of the colon. DOR signaling is enhanced during intestinal inflammation. This study demonstrates functional expression of DOR by myenteric neurons and supports the therapeutic targeting of DOR in the enteric nervous system. NEW & NOTEWORTHY DOR is activated during physiologically relevant reflex stimulation. Agonist-evoked DOR endocytosis is spatially and temporally regulated. A significant proportion of DOR is internalized in myenteric neurons during inflammation. The relative proportion of all myenteric neurons that expressed DOR and the overlap with the nNOS-positive population are increased in inflammation. DOR-specific innervation of the circular muscle is increased in inflammation, and this is consistent with enhanced responsiveness to the DOR agonist SNC80.

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Kapasi, Zoher F., Pamela A. Catlin, Jon Beck, Tamara Roehling, and Kathryn Smith. "The Role of Endogenous Opioids in Moderate Exercise Training-Induced Enhancement of the Secondary Antibody Response in Mice." Physical Therapy 81, no. 11 (2001): 1801–9. http://dx.doi.org/10.1093/ptj/81.11.1801.

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Background and Purpose. Moderate exercise training (60%–80% of maximal oxygen uptake) enhances the secondary antibody response. The mechanism underlying this enhancement, however, has not been determined. In moderate doses, endogenous opioids such as enkephalins enhance antibody response. Furthermore, serum concentrations of endogenous opioids increase in response to exercise, and training programs augment this effect. Therefore, the enhancement of the secondary antibody response induced by moderate exercise may be brought about, in part, by endogenous opioids. The purpose of this study was to examine the effects of naltrexone (an opioid antagonist) on the enhancement of secondary antibody response induced by moderate exercise in young mice. Subjects and Methods. C57BL/6 mice immunized to human serum albumin (HSA) were randomly assigned to 1 of 3 groups: naltrexone, placebo, or control (received no intervention). Then, the mice in each group were randomly assigned to either an exercise group (treadmill running at 15 m/min, 0° slope, 5 days per week for 8 weeks) or a non-exercise group. At the end of 8 weeks, booster immunization was given, and the mice in the exercise group continued to exercise. Ten days later, when high levels of antibodies are produced in secondary antibody response, anti-HSA antibodies in serum were measured by enzyme-linked immunosorbent assay (ELISA). Results. With naltrexone implantation, mice that exercised showed a depression of secondary antibody response as compared with mice that exercised and either received a placebo or did not receive any intervention. Discussion and Conclusion. Endogenous opioids may play a role in the enhancement of the secondary antibody response observed after moderate exercise.

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Venkatesan, Priya, Sunit Baxi, Cory Evans, Robert Neff, Xin Wang та David Mendelowitz. "Glycinergic Inputs to Cardiac Vagal Neurons in the Nucleus Ambiguus Are Inhibited by Nociceptin and μ-Selective Opioids". Journal of Neurophysiology 90, № 3 (2003): 1581–88. http://dx.doi.org/10.1152/jn.01117.2002.

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Most parasympathetic regulation of heart rate originates from preganglionic cardiac vagal neurons within the nucleus ambiguus. Little is known regarding the modulation of glycinergic transmission to these neurons. However, the presence of μ-opioid receptors and opioid-receptor-like (ORL1) receptors within the ambiguus, together with the presence of endogenous ligands for both receptor types in the same area, suggests opioids may modulate synaptic transmission to cardiac vagal neurons. This study therefore examined the effects of endomorphin-1 and endomorphin-2 (the μ-selective endogenous peptides), DAMGO (a synthetic, μ-selective agonist), and nociceptin (the ORL1-selective endogenous peptide) on spontaneous glycinergic inhibitory postsynaptic currents (IPSCs) in rat cardiac parasympathetic neurons. All four of the opioids used in this study decreased spontaneous IPSCs. At concentrations of 100 μM, the amplitude of the IPSCs was reduced significantly by nociceptin (–56.6%), DAMGO (–46.5%), endomorphin-1 (–45.1%), and endomorphin-2 (–26%). IPSC frequency was also significantly reduced by nociceptin (–61.1%), DAMGO (–69.9%), and endomorphin-1 (–40.8%) but not endomorphin-2. Lower concentrations of nociceptin and DAMGO (10–30 μM) also effectively decreased IPSC amplitude and frequency. The inhibitory effects of DAMGO were blocked by d-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr-NH2 (C-TOP; 10 μM), a selective μ-receptor antagonist. Neither nociceptin nor DAMGO inhibited the postsynaptic responses evoked by exogenous application of glycine or affected TTX-insensitive glycinergic mini-IPSCs. These results indicate that μ-selective opioids and nociceptin act on preceding neurons to decrease glycinergic inputs to cardiac vagal neurons in the nucleus ambiguus. The resulting decrease in glycinergic transmission would increase parasympathetic activity to the heart and may be a mechanism by which opioids induce bradycardia.

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Gomes, Ivone, Salvador Sierra, Lindsay Lueptow, et al. "Biased signaling by endogenous opioid peptides." Proceedings of the National Academy of Sciences 117, no. 21 (2020): 11820–28. http://dx.doi.org/10.1073/pnas.2000712117.

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Opioids, such as morphine and fentanyl, are widely used for the treatment of severe pain; however, prolonged treatment with these drugs leads to the development of tolerance and can lead to opioid use disorder. The “Opioid Epidemic” has generated a drive for a deeper understanding of the fundamental signaling mechanisms of opioid receptors. It is generally thought that the three types of opioid receptors (μ, δ, κ) are activated by endogenous peptides derived from three different precursors: Proopiomelanocortin, proenkephalin, and prodynorphin. Posttranslational processing of these precursors generates >20 peptides with opioid receptor activity, leading to a long-standing question of the significance of this repertoire of peptides. Here, we address some aspects of this question using a technical tour de force approach to systematically evaluate ligand binding and signaling properties ([35S]GTPγS binding and β-arrestin recruitment) of 22 peptides at each of the three opioid receptors. We show that nearly all tested peptides are able to activate the three opioid receptors, and many of them exhibit agonist-directed receptor signaling (functional selectivity). Our data also challenge the dogma that shorter forms of β-endorphin do not exhibit receptor activity; we show that they exhibit robust signaling in cultured cells and in an acute brain slice preparation. Collectively, this information lays the groundwork for improved understanding of the endogenous opioid system that will help in developing more effective treatments for pain and addiction.

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Zagon, I. S., Y. Wu, and P. J. McLaughlin. "Opioid growth factor-dependent DNA synthesis in the neonatal rat aorta." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 1 (1996): R22—R32. http://dx.doi.org/10.1152/ajpregu.1996.270.1.r22.

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In addition to neuromodulation, endogenous opioids serve as growth factors in neural and nonneural cells. This study examined the hypothesis that opioids are inhibitory growth factors in vascular development. No circadian rhythm was detected for DNA synthesis in endothelial, smooth muscle, or fibroblast cells in the aorta of 1-day-old rats. Administration of naltrexone (NTX), a potent opioid antagonist, markedly increased the labeling indexes of all three cell types. [Met5]enkephalin, found to be the only opioid peptide to influence DNA synthesis and termed the opioid growth factor (OGF), depressed DNA synthesis in each cell type for 4-6 h in a dose-dependent and receptor-mediated manner. In aortas placed in tissue culture, DNA synthesis was significantly increased by incubation in NTX and decreased by incubation with OGF, Both OGF and its receptor, zeta (zeta), were associated with the cytoplasm of all three cell types in the neonatal aorta. These results indicate that an endogenous opioid peptide (i.e., OGF) and its receptor (i.e., zeta) reside in the developing vascular cells and govern DNA synthesis, with OGF acting directly as a tonic negative regulator of cell generation in the great vessels.

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Tuulari, Jetro J., Lauri Tuominen, Femke E. de Boer, et al. "Feeding Releases Endogenous Opioids in Humans." Journal of Neuroscience 37, no. 34 (2017): 8284–91. http://dx.doi.org/10.1523/jneurosci.0976-17.2017.

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KULBERTUS, H. E. "Endogenous opioids, catecholamines and vasovagal syncope." European Heart Journal 17, no. 11 (1996): 1614–15. http://dx.doi.org/10.1093/oxfordjournals.eurheartj.a014740.

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Geffen, L. B. "Endogenous Opioids - Multiple Peptides and Actions." Australian Drug and Alcohol Review 6, S1 (1987): 41. http://dx.doi.org/10.1080/09595238780000421.

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Journal articles on the topic 'Endogenous opioids'

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