μ opioid receptor, social behaviour and autism spectrum disorder: reward matters
The endogenous opioid system is well known to relieve pain and underpin the rewarding properties of most drugs of abuse. Among opioid receptors, the μ receptor mediates most of the analgesic and rewarding properties of opioids. Based on striking similarities between social distress, physical pain an...
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Published in | British journal of pharmacology Vol. 175; no. 14; pp. 2750 - 2769 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
England
Wiley
01.07.2018
John Wiley and Sons Inc |
Subjects | |
Online Access | Get full text |
ISSN | 0007-1188 1476-5381 1476-5381 |
DOI | 10.1111/bph.13808 |
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Summary: | The endogenous opioid system is well known to relieve pain and underpin the rewarding properties of most drugs of abuse. Among opioid receptors, the μ receptor mediates most of the analgesic and rewarding properties of opioids. Based on striking similarities between social distress, physical pain and opiate withdrawal, μ receptors have been proposed to play a critical role in modulating social behaviour in humans and animals. This review summarizes experimental data demonstrating such role and proposes a novel model, the μ opioid receptor balance model, to account for the contribution of μ receptors to the subtle regulation of social behaviour. Interestingly, μ receptor null mice show behavioural deficits similar to those observed in patients with autism spectrum disorder (ASD), including severe impairment in social interactions. Therefore, after a brief summary of recent evidence for blunted (social) reward processes in subjects with ASD, we review here arguments for altered μ receptor function in this pathology.
This article is part of a themed section on Emerging Areas of Opioid Pharmacology. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.14/issuetoc |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 Contributed equally to this work. |
ISSN: | 0007-1188 1476-5381 1476-5381 |
DOI: | 10.1111/bph.13808 |