Academic literature on the topic 'Endogenous opioids'
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Journal articles on the topic "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 (March 1, 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 (March 14, 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 (August 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 (July 8, 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 (December 1, 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 (April 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 (January 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 (February 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 (February 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 (April 15, 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.
Dissertations / Theses on the topic "Endogenous opioids"
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Ghule, Aishwarya [Verfasser]. "The importance of endogenous opioids in feeding behavior / Aishwarya Ghule." Bonn : Universitäts- und Landesbibliothek Bonn, 2018. http://d-nb.info/1183093942/34.
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Stagg, Nicola Jane. "Reversal of Neuropathic Pain with Exercise is Mediated by Endogenous Opioids." Diss., The University of Arizona, 2007. http://hdl.handle.net/10150/194833.
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Exercise is often prescribed for patients with chronic pain, but there is little objective evidence supporting this recommendation. Therefore, we tested the effect of moderate aerobic exercise on the sensory hypersensitivity produced in an animal model of neuropathic pain. Male rats that underwent unilateral ligation of the L5 and L6 spinal nerves (SNL) were divided into exercise-trained or sedentary groups. Exercise training was performed using a treadmill, beginning 7 days after surgery, and continued 5 days a week for 5 weeks. Animals were exercised 30 min/day, at a speed of 14-16 m/min. Sensory testing was performed 23 hours after exercise training. Typical thermal and tactile hypersensitivity developed within 1 week after surgery. Treadmill training reversed thermal and tactile hypersensitivity in injured animals within 4 weeks, but had no effect on sham-operated or non-operated animals. One week after the cessation of exercise training, tactile hypersensitivity returned.The effects of exercise training on SNL-induced sensory hypersensitivity were reversed by the opioid receptor antagonist naloxone. Naloxone or naloxone methiodide reversed the effects of exercise when administered intracerebroventricularly (i.c.v.). Immunohistochemistry revealed increased immunostaining for B-endorphin and met-enkephalin in the periaquaductal grey (PAG) and rostral ventromedial medulla (RVM) regions of exercise-trained animals compared to sedentary animals. An ELISA immunoassay revealed a 31% increase in PAG B-endorphin content in exercise-trained SNL animals. More BDNF was also present in the brain's of exercise-trained animals compared to sedentary, specifically in the ventromedial hypothalamus, hippocampus, and outer rim of the PAG. Administering a BDNF sequestering agent reversed B-endorphin increases in the PAG of exercise-trained animals. Exercise-trained SNL animals treated with 25 ug BDNF sequestering agent (i.c.v.) had lower tactile thresholds compared to the exercise-trained vehicle group.These results support the recommendation of moderate aerobic exercise for patients suffering from neuropathic pain, and suggest that exercise-induced pain reversal results from the upregulation of endogenous opioids in the brainstem. Additionally, increased BDNF with exercise training may play a role in exercise-induced reversal of neuropathic pain by increasing the expression of endogenous opioids, but this needs to be verified further.
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Robinson, Kathleen Clare. "Cutaneous Biology and Endogenous Opioids: How the Skin Modulates Pain and Addiction." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11215.
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The Proopiomelanocortin gene, (POMC), produces many biologically active peptides including the endogenous opioid, β-endorphin, and the melanocortins: α-Melanocyte Stimulating Hormone, (αMSH), γMSH, βMSH and Adrenocorticotropic Hormone, (ACTH). βendorphin is released by the brain in response to stress or injury and is a potent analgesic. Melanocortins are well known for regulating pigmentation, metabolism, and cortisol levels. Additionally, opioids and melanocortins are known to have opposing actions in several settings including the regulation of pain and metabolism. The Melanocyte Stimulating Hormones are expressed in the skin where they bind the Melanocortin 1 Receptor on melanocytes and promote pigmentation. It has been reported that β-endorphin is also produced in the skin, however it was not believed to have a central effect. In this thesis I show that expression of these peptides in the skin is reflected in blood levels and affects nociception and behavior.
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au, Ash_Frew@yahoo com, and Ashley Kim Frew. "The influence of discouragement, anxiety and anger on pain: An examination of the role of endogenous opioids." Murdoch University, 2005. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20050930.111852.
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Animal research suggests that exposure to inescapable stressors can lead to an endogenous opioid-mediated form of pain inhibition, known as stress-induced analgesia (SIA). Similar results have been found with humans, although the literature is much less extensive and at times contradictory where uncontrollable stressors have led to an increase, rather than a decrease in pain. More recently, there has been some suggestion that emotions play an important role in pain modulation, and that particular negative moods are associated with opioid-mediated hypoalgesia. This research aimed to clarify the psychological (cognitive and affective) factors underlying endogenous opioid-mediated pain inhibition in humans.
The purpose of Study 1 was to examine the effects of stressor controllability and predictability on pain intensity (PI) and unpleasantness (UP) ratings during a cold pressor task (CPT) in 56 male and female subjects. The stressor involved a timed mental arithmetic task during which three moderately noxious electrical shocks were delivered. Although subjects were informed that shock delivery was contingent on math performance, the shock schedule was preset and identical across conditions. Perceived control over the shocks was manipulated between subjects by altering the difficulty of the math task. Shock predictability was manipulated by changing the colour of the computer screen to warn of an impending shock. Subjects were randomly allocated to four experimental conditions (controllable-predictable, controllable-unpredictable, uncontrollable-predictable, and uncontrollable-unpredictable shocks). Visual analogue ratings of perceived self-efficacy (to avoid the shocks) and mood (anxiety, confusion, discouragement, anger, sluggishness, liveliness) were completed before, during and after the math task. Significantly greater discouragement and lower self-efficacy was reported in uncontrollable conditions indicating that controllability was manipulated effectively. Results indicated that a perceived lack of control over shocks during the math task led to significantly greater decreases in PI, but not UP, ratings during the last stages of a 4-minute fixed interval CPT after the math task. Shock predictability failed to influence subjective pain ratings alone; however, unpredictability interacted with lack of control to initially increase pain, followed by analgesia. Stress-induced increases in negative affect (anxiety, discouragement, anger) were associated with decreases in cold pressor PI, but with increased shock PI and UP during the math task. It was concluded that lack of control over an aversive event and negative affect led to SIA during a prolonged pain stimulus, whereas shock predictability had little influence
on pain.
In Study 2, 70 male and female subjects received either an opioid antagonist (naltrexone) or a placebo before the math task (using a double-blind, counterbalanced design), in order to determine the role of endogenous opioids in SIA. Subjects were randomly assigned to one of three experimental conditions to investigate whether the shocks themselves may have contributed to analgesia observed after the math task: (1) easy task-few shocks, (2) hard task-few shocks,
(3) hard task-many shocks. Increases in systolic blood pressure (SBP), diastolic blood pressure (DBP), anxiety, anger and discouragement indicated that negative affect and sympathetic arousal were induced during the math task. Endogenous opioids inhibited the rise in anger, but not discouragement or anxiety, during the math task. There was some evidence that perceived lack of control over shocks, and not the shocks themselves, led to opioid-mediated decreases in cold pressor UP after the math task. In correlational analyses, discouraged subjects under opioid blockade reported more cold pressor UP after the math task than their placebo counterparts. However, this effect was not strong enough to reach statistical significance in regression analyses. Anxiety, anger, discouragement and lack of control over shocks increased shock PI and UP during the math task.
A growing body of research with normotensive subjects has linked increased cardiovascular activity with insensitivity to pain, but the role of endogenous opioids remains contentious. In addition to the investigations outlined above, Study 2 aimed to examine the contribution of endogenous opioids in the cardiovascular-pain relationship. However, there was no evidence of an interaction between pain and cardiovascular activity in this study.
Study 3 was carried out to investigate opioid involvement in the effects of an uncontrollable stressor and stress-induced negative mood on cold pressor PI, UP and pain tolerance, and onset/thresholds of the nociceptive flexion reflex (RIII). Forty-three male and female subjects were administered either naltrexone or a placebo using a double-blind, counterbalanced design before completing a timed mental arithmetic stressor (identical to the hard task-many shocks condition in Study 2). Increases in physiological (SBP, DBP) and affective measures (anxiety, anger and discouragement) indicated that the math task induced a marked state of stress. Negative affect increased shock PI and UP during the task, whereas self-efficacious subjects taking the placebo experienced less shock pain. However, uncontrollable stress led to an opioid-antagonised increase in cold pressor UP. Stressor controllability had a similar, but marginal, effect on cold pressor PI, but not pain tolerance. Tolerance of cold pressor pain was not associated with subjective PI and UP ratings, but was positively associated with endurance to non-painful, but unpleasant tasks (Valsalva Manoeuvre, Letter-Symbol Matching Task), indicating that pain tolerance was measuring the ability to tolerate discomfort, in addition to pain. Results of hierarchical multiple regressions demonstrated that increases in discouragement were positively related to increases in cold pressor UP after the math task, for naltrexone recipients only. These findings suggest that discouragement inhibits the UP of a prolonged pain stimulus via opioid mechanisms. RIII latencies and thresholds were not affected by the math task or by opioid blockade; however, these null effects may be due to methodological limitations. Unlike Study 2, higher blood pressure was associated with shock and cold pressor pain inhibition in normotensive subjects, and this relationship appeared to be mediated by opioids.
The strong association between chronic pain and depression has led to speculation that the endogenous opioid system and pain modulatory mechanisms may be impaired in depression. At the time that this research was carried out, no studies had examined whether this was the case. In Study 4, the effect of a cognitive stressor (math task used in Study 3) on foot cold pressor PI, UP and pain tolerance and the nociceptive, or R2 component, of the blink reflex was investigated in 61 participants with or without major depression (as met by DSM-IV diagnostic criteria and confirmed by psychometric testing). Naltrexone or placebo was administered to subjects an hour before the math task using a double-blind, counterbalanced design. Increases in physiological (SBP, DBP) and affective measures (anxiety, anger and discouragement) confirmed that the math task induced the targeted emotional state. An opioid-mediated reduction in anxiety occurred mid-way through the math task. Opioid-mediated decreases in foot cold pressor PI and UP were observed in depressed and non-depressed subjects after the math task. R2 onset to 10 mA was facilitated after the task regardless of opioid blockade, suggesting that endogenous opioids are not involved in the modulation of the BR. Increased anxiety and discouragement led to opioid-mediated inhibition of shock PI and UP during the task and, to a lesser extent, foot cold pressor PI and UP after the math task. Anger increased shock pain without being influenced by opioid blockade. Pain tolerance was not influenced by depression, opioid blockade or mood. These findings failed to support the idea that SIA is impaired in major depression, suggesting instead that uncontrollable aversive events and negative mood (anxiety, discouragement) lead to opioid activation and insensitivity to acute pain. Multiple regression analyses revealed that the inverse relationship between resting blood pressure and foot cold pressor PI and UP was opioid-mediated in controls only, suggesting that opioid dysregulation in depression might influence regulatory functions other than SIA.
In Study 4, opioid involvement in hetero-segmental pain inhibitory phenomena termed diffuse noxious inhibitory controls (DNIC) was examined separately, before psychological stress. Specifically, the effect of a heterotopic noxious conditioning stimulus (CS i.e., hand CPT) on R2 onset latency was compared before and after drug absorption (before the math task). An inhibitory effect of the first CS was detected at each electrical stimulus intensity consistent with a DNIC effect. However, this effect was not detected during the second CS, suggesting that some other process masked the DNIC effect.
In summary, the findings indicate that uncontrollable aversive events and negative emotion (primarily discouragement) activates endogenous opioids and inhibits pain in human subjects, whether depressed or not. Notably, opioids inhibited the affective component of pain perception, or pain UP, more consistently than PI, suggesting that the antinociceptive function of opioids may be secondary to an important emotional-modulatory role. Endogenous opioids also appeared to mediate the cardiovascular-pain relationship in normotensive non-depressed subjects, suggesting an important stress-regulatory role for these peptides. Opioid-mediated masking of this relationship in major depression suggests that functioning of the endogenous opioid system may be impaired in baroreceptor-mediated analgesia. This finding provides preliminary support for the notion that opioid antinociceptive system dysfunction may contribute to cardiovascular disease in depression.
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Gustafsson, Lisa. "Endogenous Opioids and Voluntary Ethanol Drinking : Consequences of Postnatal Environmental Influences in Rats." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7776.
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Daoura, Loudin. "Early Environment and Adolescent Ethanol Consumption : Effects on Endogenous Opioids and Behaviour in Rats." Doctoral thesis, Uppsala universitet, Institutionen för farmaceutisk biovetenskap, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-198670.
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Excessive and compulsive ethanol drinking is one of the most serious public health issues. Therefore, it is vital to increase the knowledge about risks and protection for alcohol use disorders (AUD) to optimize prevention and treatment strategies. Ethanol consumption commonly initiates during adolescence when extensive neuronal maturation and development also occurs. Early exposure to ethanol is a risk factor for AUD, but the effects of adolescent drinking and the basis for the individual susceptibility to AUD are not fully understood. The interactions between genotype and environmental factors determine the individual risk for AUD and this thesis aimed to examine the environmental impact. The specific aims were to investigate 1) how early-life conditions affect adolescent voluntary ethanol drinking, behavioural profiles, endogenous opioids and response to treatment with an opioid antagonist (naltrexone), and 2) whether alterations detected in the offspring may be mediated by variations in maternal behaviour. A rodent maternal separation (MS) model was used to mimic a protective and risk-inducing early-life environment, respectively, with the use of 15 min (MS15) or 360 min (MS360) of daily MS. The main findings were 1) the MS360, but not the MS15 rats, responded to naltrexone following adolescent ethanol drinking; all adolescent rats had a high voluntary ethanol intake independent of early environmental conditions whereas in the adult groups the MS360, but not the MS15 rats, increased their ethanol intake and preference over time; adolescent ethanol exposure resulted in higher dynorphin levels in hippocampus and higher Met-enkephalin-Arg6Phe7 in the amygdala, independently of rearing conditions, 2) behavioural profiling using the multivariate concentric square field™ test showed: the young MS360 rats had increased risk assessment and risk taking behaviour compared to the young MS15 rats; the young MS15 rats increased, whereas the young MS360 rats decreased, their risk assessment and risk taking behaviour over time; differences in pup-retrieval strategies where the MS360 dams retrieved some pups into a safe area but as compared to MS15 rats they left more pups in a risk area; increased risk assessment behaviour in the MS360 dams immediately after weaning. Taken together, early-life environmental conditions alter adult but not adolescent drinking, the response to naltrexone, and behaviour in dams and offspring. Adolescent rats consumed more ethanol independent of rearing conditions and displayed increased opioid levels in brain areas related to cognition and addiction.
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Olson, Keith Mathew, and Keith Mathew Olson. "Atypical Opioid Interactions – Development of Selective Mu-Delta Heterodimer Antagonists, Clinical Opioids at Non-Mu Pain Targets and Endogenous Biased Signaling." Diss., The University of Arizona, 2017. http://hdl.handle.net/10150/626669.
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Most clinical opioids produce analgesia through the Mu Opioid Receptor (MOR) providing the only effective treatment for chronic pain patients. These studies explore three pre-clinical strategies to improve MOR analgesia and minimize side effects: 1) compounds that target G-protein Coupled Receptors (GPCRs) heterodimers, such as heterodimerization between the Delta Opioid Receptor (DOR) and MOR (MDOR); 2) multi-functional compounds that target multiple receptor systems for synergistic effects, such as a MOR agonist and a the serotonin reuptake transporter (SERT) inhibitor; or 3) biased agonists that preferentially activate one signaling pathway associated with analgesia over another associated with side effects at the same receptor.
First, several indirect lines of evidence indicate the MOR-DOR heterodimer (MDOR) can regulate MOR opioid tolerance and withdrawal. However, studying MDOR remains difficult because no selective MDOR antagonists are available. To address this need, we created a novel series of bivalent MDOR antagonists by connecting a low affinity MOR antagonist (H-Tyr-Pro-Phe-D1Nal-NH2) to a moderate affinity DOR (H- Tyr-Tic-OH) antagonist with variable length polyamide spacers (15-41 atoms). In vitro radioligand binding and [35S]-GTPγS coupling assays in MOR, DOR, and MDOR expressing cell lines show bivalent ligands produce a clear length dependence in MDOR but not MOR or DOR cell lines. The lead compound – D24M with a 24-atom spacer – displayed high potency (IC50MDOR = 0.84 nM) with 91-fold selectivity for MDOR:DOR and 1,000-fold MDOR:MOR selectivity.
Second, clinicians have long appreciated subtle but distinct differences in analgesia and side effects of MOR opioids. A variety of non-MOR targets including DOR, Kappa Opioid Receptor (KOR), the Cannabinoid Receptor-1 (CB1), the Sigma-1 Receptor (σ1R), the Dopamine- (DAT), Serotonin- (SERT) and Norepinephrine- Reuptake Transporters (NET) induce analgesia and/or modulate MOR mediated side effects. To determine if different opioid profiles arise from non-MOR interactions, we evaluated the binding and function of nine clinical analgesics at the nine aforementioned targets revealing several clinical opioids contain previously unidentified affinity’s or activity’s. Hydrocodone displayed low affinity at the MOR (KI = 1800 nM) and only ~2 fold less affinity at the σ1R (KI = 4000 nM). Second buprenorphine promoted monoamine influx at DAT, SERT and NET with EC50 > 1,000 nM. These novel interactions suggest the nuanced differences of clinical opioids may arise from previously unappreciated off-target effects. Future studies will assess whether these in vitro results predict hydrocodone and buprenorphine activity in vivo.
Finally, the unique function of the numerous endogenous opioid peptides at a given receptor remains unclear. How endogenous ligands interact with ORs produces obvious drug design consequences. These studies show two endogenous Dynorphin analogues – Dynorphin A and Dynorphin B – differentially regulate two ubiquitous signaling modules – βarrestin2 and Gαi/o– at the DOR. Dynorphin A and Dynorphin B swap potency rank orders for β-arrestin2 recruitment and [35S]-GTPγS signaling, indicating two distinct signaling platforms are formed. Dynorphin A but not Dynorphin B treatment simulated AC super activation, while Dynoprhin B internalized DOR better than Dynorphin A. These in vitro assays suggest endogenous Dynorphin analogues differentially regulate signals at the DOR in vitro. Future work includes further characterizing signaling differences in vitro and testing these changes in vivo.
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Schwellnus, Martin Peter. "The role of the endogenous opioid system in thermoregulation during exercise." Master's thesis, University of Cape Town, 1988. http://hdl.handle.net/11427/27169.
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In man the metabolic heat produced during physical exercise stresses the thermoregulatory system, particularly if hot, humid environmental conditions prevail. It has recently been postulated that endogenous opioids may play a role in regulating body temperature at rest and because it has also been shown that blood levels of these substances increase during exercise, the possibility exists that endogenous opioids may play a role in thermoregulation during exercise. A study was conducted in two parts to determine the thermoregulatory response during exercise with and without pharmacologic blockade of the opioid receptor. In Part I nine healthy male subjects performed 30 minutes cycling at 50 % maximal aerobic capacity in an environmentally controlled laboratory. The subjects received either placebo, 2mg or 10mg naloxone hydrochloride in a randomized double-blind crossover fashion prior to the exercise test. Rectal temperatures were recorded at one-minute intervals and cardiorespiratory parameters were measured during the test. Water loss was calculated from differences in nude body weight. In part II eight male subjects performed a graded maximal cycle ergometer test after receiving either placebo or 2mg naloxone in a randomized double-blind crossover fashion. Rectal and sublingual temperatures were recorded before and after the test and oesophageal temperature was recorded at one-minute intervals during the test. Cardiorespiratory parameters were recorded during the test. The results of Part I show that rises in rectal temperature as well as calculated water losses were similar for placebo and after the administration of both 2mg and 10mg naloxone. Similarly, during maximal exercise (Part II) the rise in rectal and oesophageal temperatures was equivalent for placebo and 2mg naloxone but sublingual temperature failed to rise during exercise following the 2mg naloxone dose. Cardiorespiratory responses did not differ between placebo and naloxone tests in both Part I and Part II of the study. These results indicate that naloxone-mediated blockade of opioid receptors does not affect rectal and oesophageal temperature responses to either submaximal or maximal exercise. Naloxone appears to selectively alter the sublingual temperature response to exercise possibly by altering local blood flow. It is concluded that insofar as naloxone induced opioid receptor blockade provides a measure of the function of the endogenous opioid system, this study suggests that the endogenous opioid system does not play a significant role in thermoregulation during exercise.
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Frew, Ashley. "The influence of discouragement, anxiety and anger on pain : an examination of the role of endogenous opioids /." Access via Murdoch University Digital Theses Project, 2004. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20050930.111852.
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Frew, Ashley Kim. "The influence of discouragement, anxiety and anger on pain: an examination of the role of endogenous opioids." Thesis, Frew, Ashley Kim (2005) The influence of discouragement, anxiety and anger on pain: an examination of the role of endogenous opioids. PhD thesis, Murdoch University, 2005. https://researchrepository.murdoch.edu.au/id/eprint/55/.
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Animal research suggests that exposure to inescapable stressors can lead to an endogenous opioid-mediated form of pain inhibition, known as stress-induced analgesia (SIA). Similar results have been found with humans, although the literature is much less extensive and at times contradictory where uncontrollable stressors have led to an increase, rather than a decrease in pain. More recently, there has been some suggestion that emotions play an important role in pain modulation, and that particular negative moods are associated with opioid-mediated hypoalgesia. This research aimed to clarify the psychological (cognitive and affective) factors underlying endogenous opioid-mediated pain inhibition in humans.
The purpose of Study 1 was to examine the effects of stressor controllability and predictability on pain intensity (PI) and unpleasantness (UP) ratings during a cold pressor task (CPT) in 56 male and female subjects. The stressor involved a timed mental arithmetic task during which three moderately noxious electrical shocks were delivered. Although subjects were informed that shock delivery was contingent on math performance, the shock schedule was preset and identical across conditions. Perceived control over the shocks was manipulated between subjects by altering the difficulty of the math task. Shock predictability was manipulated by changing the colour of the computer screen to warn of an impending shock. Subjects were randomly allocated to four experimental conditions (controllable-predictable, controllable-unpredictable, uncontrollable-predictable, and uncontrollable-unpredictable shocks). Visual analogue ratings of 'perceived self-efficacy' (to avoid the shocks) and mood (anxiety, confusion, discouragement, anger, sluggishness, liveliness) were completed before, during and after the math task. Significantly greater discouragement and lower self-efficacy was reported in 'uncontrollable' conditions indicating that 'controllability' was manipulated effectively. Results indicated that a perceived lack of control over shocks during the math task led to significantly greater decreases in PI, but not UP, ratings during the last stages of a 4-minute fixed interval CPT after the math task. Shock predictability failed to influence subjective pain ratings alone; however, unpredictability interacted with lack of control to initially increase pain, followed by analgesia. Stress-induced increases in negative affect (anxiety, discouragement, anger) were associated with decreases in cold pressor PI, but with increased shock PI and UP during the math task. It was concluded that lack of control over an aversive event and negative affect led to SIA during a prolonged pain stimulus, whereas shock predictability had little influence
on pain.
In Study 2, 70 male and female subjects received either an opioid antagonist (naltrexone) or a placebo before the math task (using a double-blind, counterbalanced design), in order to determine the role of endogenous opioids in SIA. Subjects were randomly assigned to one of three experimental conditions to investigate whether the shocks themselves may have contributed to analgesia observed after the math task: (1) easy task-few shocks, (2) hard task-few shocks, (3) hard task-many shocks. Increases in systolic blood pressure (SBP), diastolic blood pressure (DBP), anxiety, anger and discouragement indicated that negative affect and sympathetic arousal were induced during the math task. Endogenous opioids inhibited the rise in anger, but not discouragement or anxiety, during the math task. There was some evidence that perceived lack of control over shocks, and not the shocks themselves, led to opioid-mediated decreases in cold pressor UP after the math task. In correlational analyses, discouraged subjects under opioid blockade reported more cold pressor UP after the math task than their placebo counterparts. However, this effect was not strong enough to reach statistical significance in regression analyses. Anxiety, anger, discouragement and lack of control over shocks increased shock PI and UP during the math task.
A growing body of research with normotensive subjects has linked increased cardiovascular activity with insensitivity to pain, but the role of endogenous opioids remains contentious. In addition to the investigations outlined above, Study 2 aimed to examine the contribution of endogenous opioids in the cardiovascular-pain relationship. However, there was no evidence of an interaction between pain and cardiovascular activity in this study.
Study 3 was carried out to investigate opioid involvement in the effects of an uncontrollable stressor and stress-induced negative mood on cold pressor PI, UP and pain tolerance, and onset/thresholds of the nociceptive flexion reflex (RIII). Forty-three male and female subjects were administered either naltrexone or a placebo using a double-blind, counterbalanced design before completing a timed mental arithmetic stressor (identical to the 'hard task-many shocks' condition in Study 2). Increases in physiological (SBP, DBP) and affective measures (anxiety, anger and discouragement) indicated that the math task induced a marked state of stress. Negative affect increased shock PI and UP during the task, whereas self-efficacious subjects taking the placebo experienced less shock pain. However, uncontrollable stress led to an opioid-antagonised increase in cold pressor UP. Stressor controllability had a similar, but marginal, effect on cold pressor PI, but not pain tolerance. Tolerance of cold pressor pain was not associated with subjective PI and UP ratings, but was positively associated with endurance to non-painful, but unpleasant tasks (Valsalva Manoeuvre, Letter-Symbol Matching Task), indicating that pain tolerance was measuring the ability to tolerate discomfort, in addition to pain. Results of hierarchical multiple regressions demonstrated that increases in discouragement were positively related to increases in cold pressor UP after the math task, for naltrexone recipients only. These findings suggest that discouragement inhibits the UP of a prolonged pain stimulus via opioid mechanisms. RIII latencies and thresholds were not affected by the math task or by opioid blockade; however, these null effects may be due to methodological limitations. Unlike Study 2, higher blood pressure was associated with shock and cold pressor pain inhibition in normotensive subjects, and this relationship appeared to be mediated by opioids.
The strong association between chronic pain and depression has led to speculation that the endogenous opioid system and pain modulatory mechanisms may be impaired in depression. At the time that this research was carried out, no studies had examined whether this was the case. In Study 4, the effect of a cognitive stressor (math task used in Study 3) on foot cold pressor PI, UP and pain tolerance and the nociceptive, or R2 component, of the blink reflex was investigated in 61 participants with or without major depression (as met by DSM-IV diagnostic criteria and confirmed by psychometric testing). Naltrexone or placebo was administered to subjects an hour before the math task using a double-blind, counterbalanced design. Increases in physiological (SBP, DBP) and affective measures (anxiety, anger and discouragement) confirmed that the math task induced the targeted emotional state. An opioid-mediated reduction in anxiety occurred mid-way through the math task. Opioid-mediated decreases in foot cold pressor PI and UP were observed in depressed and non-depressed subjects after the math task. R2 onset to 10 mA was facilitated after the task regardless of opioid blockade, suggesting that endogenous opioids are not involved in the modulation of the BR. Increased anxiety and discouragement led to opioid-mediated inhibition of shock PI and UP during the task and, to a lesser extent, foot cold pressor PI and UP after the math task. Anger increased shock pain without being influenced by opioid blockade. Pain tolerance was not influenced by depression, opioid blockade or mood. These findings failed to support the idea that SIA is impaired in major depression, suggesting instead that uncontrollable aversive events and negative mood (anxiety, discouragement) lead to opioid activation and insensitivity to acute pain. Multiple regression analyses revealed that the inverse relationship between resting blood pressure and foot cold pressor PI and UP was opioid-mediated in controls only, suggesting that opioid dysregulation in depression might influence regulatory functions other than SIA.
In Study 4, opioid involvement in hetero-segmental pain inhibitory phenomena termed diffuse noxious inhibitory controls (DNIC) was examined separately, before psychological stress. Specifically, the effect of a heterotopic noxious conditioning stimulus (CS i.e., hand CPT) on R2 onset latency was compared before and after drug absorption (before the math task). An inhibitory effect of the first CS was detected at each electrical stimulus intensity consistent with a DNIC effect. However, this effect was not detected during the second CS, suggesting that some other process masked the DNIC effect.
In summary, the findings indicate that uncontrollable aversive events and negative emotion (primarily discouragement) activates endogenous opioids and inhibits pain in human subjects, whether depressed or not. Notably, opioids inhibited the affective component of pain perception, or pain UP, more consistently than PI, suggesting that the antinociceptive function of opioids may be secondary to an important emotional-modulatory role. Endogenous opioids also appeared to mediate the cardiovascular-pain relationship in normotensive non-depressed subjects, suggesting an important stress-regulatory role for these peptides. Opioid-mediated masking of this relationship in major depression suggests that functioning of the endogenous opioid system may be impaired in baroreceptor-mediated analgesia. This finding provides preliminary support for the notion that opioid antinociceptive system dysfunction may contribute to cardiovascular disease in depression.
Books on the topic "Endogenous opioids"
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Holaday, John W. Endogenous opioids and their receptors. Kalamazoo, Mich: Upjohn, 1985.
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Marcello, Negri, Lotti G, and Grossman Ashley, eds. Clinical perspectives of endogenous opioids production. Chichester: J. Wiley, 1992.
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Browning, Andrew J. F. Endogenous opioid peptides and human reproduction. Birmingham: University of Birmingham, 1985.
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Salansky, Norman. Endogenous opioid peptide level changes under electrostimulation and their assessment by the EEG. Downsview, Ontario: [s.n.], 1994.
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Sommer, Claudia. Endogenous opioids mediate stress-induced analgesia. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0031.
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This chapter reviews the landmark paper published in 1990 by Stein et al. and entitled ‘Opioids from immunocytes interact with receptors on sensory nerves to inhibit nociception in inflammation’. Opioids, besides acting centrally as analgesics, may act peripherally upon opioid receptors located on axons and on immune cells. In the publication by Stein et al., it was shown for the first time that endogenous opioid peptides released from immune cells mediate stress-induced analgesia, potentially through opioid receptors on peripheral nerve endings. This finding has led to numerous follow-up studies on endogenous analgesia, including work showing that cannabinoid analgesia is mediated via the peripheral release of opioids, and to the concept of topical opioid analgesia, which may be a good way of using the potent analgesia that opioids can convey, without their CNS-associated side effects.
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Dickenson, Tony. Endogenous opioids in the CNS. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0019.
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This short and concise paper was the first to unequivocally reveal that there were endogenous opioids in the central nervous system (CNS), identify their peptide nature and sequence, and show that they exerted physiological inhibitory effects. The idea that there were natural opioids fitted with concurrent reports of opiate-binding sites, and this led to the description of multiple receptors with their own families of peptide transmitters. No truly novel opioid drugs have emerged since, and attempts to protect and manipulate the enkephalins for pain control have yet to be successful. This does not detract from this key study, which made us think about pain modulation in a different way, and subsequent work has clearly shown how endogenous opioid signalling is critical in CNS function, perhaps most importantly in endogenous pain control, such as that harnessed by placebo analgesia.
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Taylor, Véronique A., and Pierre Rainville. Endogenous opioids in placebo-induced analgesia. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0011.
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Placebos achieve scientifically proven pain-relieving effects yet are inactive substances for the treatment of pain. Levine, Gordon, and Fields were the first to demonstrate the role of endogenous opioids in placebo-induced analgesia during dental post-operative pain. Several studies using pharmacological manipulations and/or neuroimaging techniques confirmed their findings that placebo analgesia is reversible by naloxone, and also identified brain pathways involved in opioidergic neurotransmission during placebo analgesia (prefrontal regions rich in opioid receptors such as the anterior cingulate cortex, presumably initiating descending pain modulation through downstream projections to the brainstem). Fifty years of research in pharmacology and neurobiology have contributed to the identification of physical as well as psychological determinants of placebo analgesia. Expectations of pain relief are maintained by conditioned learning and reward-related processes, reflected by interactions between different neurotransmitters (opioids, dopamine, endocannabinoids) in a variety of brain circuits related to executive/cognitive processes as well as affect and reward.
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Bird, Mark F., and David G. Lambert. Deorphanization of ORL-1/LC132 by reverse pharmacology in two landmark studies. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0026.
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Deorphanization of ORL-1/LC132 in 1995 by reverse pharmacology in two simultaneously published landmark studies added a new member to the opioid family of G-protein coupled receptors. Meunier and Reinscheid used cells expressing recombinant ORL-1 (human) or LC132 (rat) and the presumed intracellular inhibition of cyclic AMP formation to ‘fish’ for endogenous peptide ligands in rat whole-brain and pig hypothalamic extracts. Both studies reported the isolation of a 17-amino-acid peptide, which was named nociceptin and orphanin FQ by the two authors, respectively. The behaviour of the isolated peptide was a complete surprise, as a general hyperalgesia was observed when the peptide was administered at supraspinal sites. We now know that this peptide has, in fact, anti-opioid action, particularly in the medulla. The endogenous peptide exerts a multitude of effects both in the nervous system and, unlike classical opioids, has efficacy in neuropathic pain.
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Bromley, Lesley. The molecular basis for the placebo effect. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0041.
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The landmark paper discussed in this chapter is ‘The neurobiology of placebo analgesia: From endogenous opioids to cholecystokinin’, published by Benedetti and Amanzio in 1997. This major review considered the placebo and nocebo effect in a more scientific framework compared to previous treatise of a nebulous concept whose only role is to act as a comparator for controlled trials. By expounding robust evidence, Benedetti and Amanzio added credence to the placebo effect, with not just psychological but also physiological data, acknowledging it as an effective therapeutic action. Furthermore, the importance of endogenous opioids and cholecystokinin in the mechanism of placebo were put into sharp relief, giving an intuitive basis and scientific validation to this effect.
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Simon, Eric J., and Hiroshi Takagi. Advances in Endogenous and Exogenous Opioids: Proceedings of the International Narcotic Research Conference Held in Kyoto, Japan on July 26-30 1981. Elsevier, 2013.
Find full textBook chapters on the topic "Endogenous opioids"
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Berezniuk, Iryna, and Lloyd D. Fricker. "Endogenous Opioids." In The Opiate Receptors, 93–120. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-993-2_5.
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Spector, S., and J. Donnerer. "Presence of Endogenous Opiate Alkaloids in Mammalian Tissues." In Opioids, 295–304. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77460-7_13.
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Khachaturian, H., M. K. H. Schaefer, and M. E. Lewis. "Anatomy and Function of the Endogenous Opioid Systems." In Opioids, 471–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77460-7_20.
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Blatteis, C. M., and A. A. Romanovsky. "Endogenous Opioids and Fever." In Thermal Balance in Health and Disease, 435–41. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-7429-8_61.
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McCubbin, James A. "Endogenous Opioids/Endorphins/Enkephalin." In Encyclopedia of Behavioral Medicine, 766–69. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_247.
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LaCaille, Lara, Anna Maria Patino-Fernandez, Jane Monaco, Ding Ding, C. Renn Upchurch Sweeney, Colin D. Butler, Colin L. Soskolne, et al. "Endogenous Opioids/Endorphins/Enkephalin." In Encyclopedia of Behavioral Medicine, 687–90. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_247.
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McCubbin, James A. "Endogenous Opioids/Endorphins/Enkephalin." In Encyclopedia of Behavioral Medicine, 1–4. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4614-6439-6_247-2.
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Carr, D. B., and S. M. Fishman. "EXERCISE AND ENDOGENOUS OPIOIDS." In Exercise Endocrinology, edited by K. Fotherby and S. B. Pal, 157–82. Berlin, Boston: De Gruyter, 1985. http://dx.doi.org/10.1515/9783110866483-010.
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Papini, Mauricio R., and Leonardo A. Ortega. "Endogenous Opioids, Opioid Receptors, and Incentive Processes." In Handbook of Behavior, Food and Nutrition, 1011–19. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-92271-3_66.
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Faden, A. I. "Role of Endogenous Opioids in Central Cardiovascular Regulation and Dysregulation." In Opioids II, 191–204. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77540-6_8.
Full textConference papers on the topic "Endogenous opioids"
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Gifford, Alex H., Laurie A. Waterman, Joseph Ward, John Baird, and Donald A. Mahler. "Neuromodulatory Effect Of Endogenous Opioids On The Intensity And Unpleasantness Of Breathlessness In COPD." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5806.
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Ekstrom, M. P., T. Hunt, S. Louw, D. J. Eckert, P. Allcroft, T. To, M. Krajnik, D. A. Mahler, and D. Currow. "The Effect of Endogenous Opioids on the Peripheral Modulation of Breathlessness in People with Moderate to Severe COPD." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5741.
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Mangani, Davide, Linglin Huang, Meromit Singer, Ruitong Li, Rocky Barilla, Giulia Escobar, Katherine Tooley, et al. "964 Dynamic immune landscapes during melanoma progression reveal a role for endogenous opioids in driving T cell dysfunction." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0964.
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Olson, Keith M., Justin Lavigne, John Streicher, Frank Porreca, and Victor J. Hruby. "Differential Potencies for Endogenous Dynorphins Indicate Functional Selectivity at the Delta Opioid Receptor." In The 24th American Peptide Symposium. Prompt Scientific Publishing, 2015. http://dx.doi.org/10.17952/24aps.2015.223.
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Nazarova, G. A., N. G. Bogdanova, E. V. Alekseeva, and S. K. Sudakov. "INTERMITTENT USE OF SOLUTIONS OF GLUCOSE, SODIUM CHLORIDE AND MONOSODIUM GLUTAMATE CAUSES ENDOGENOUS OPIOID DEPENDENCE." In MODERN PROBLEMS IN SYSTEMIC REGULATION OF PHYSIOLOGICAL FUNCTIONS. NPG Publishing, 2019. http://dx.doi.org/10.24108/5-2019-confnf-59.
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Fabri, Júlia Campos, Maria Julia Filgueiras Granato, Maria Clara Lopes Rezende, Maria Luiza Franco de Oliveira, and Leandro de Souza Cruz. "The impact of genetic polymorphism in pain mechanisms." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.708.
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Background:Variations in genes codifying target structures in the nociceptive pathway can result in pain attenuation or increase.Objective:Investigate the genetic polymorphism influence in the individual pain threshold. Methods: Search on PubMed with the terms “genetic”, “pain” and its synonyms published in the last 10 years. Results:The subjective and individual mechanisms of pain aren’t completely understood, but genetic susceptibility is one of the hypothesis to explain these differences.The KCNK18 gene influences the synaptic transmission by producing potassium channel protein that equalizes resting membrane potential, calcineurin activated and inhibited by arachidonic acid. This gene was found more frequently in migraine individuals. The COMT gene increase the sensibility to pain by met-enkephalins reduction and/or catecholamine elevation. Its activity’s reduced in fibromyalgia patients. However, the OPRM1 gene, an opioid receptor, was found in individuals with a higher pain threshold.Furthermore, studies with human cell culture shows the analgesic role of the gene A118G, by its greater binding affinity for β-endorphin.It is associated with more effective endorphinergic endogenous pain inhibition. Conclusion:Researches indicates a striking participation of genetic polymorphism in pain mechanisms. The knowledge about genetic variables on pain perception can contribute to the development of individualized analgesic protocols and therapeutic strategies, accordantly to the patient genetic profile. This evolution becomes fundamental in a population that tend to the indiscriminate use of analgesics.