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© Uwe Maskos
Tranche d'hippocampe de souris colorée avec deux toxines spécifiques de sous-types de récepteur nicotinique, en rouge (grains), et en vert (corps cellulaires). L'hippocampe est la zone du cerveau qui gère la mémoire spatiale.
Publication : British journal of pharmacology

The α3β4* nicotinic ACh receptor subtype mediates physical dependence to morphine: mouse and human studies

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in British journal of pharmacology - 01 Aug 2014

Muldoon PP, Jackson KJ, Perez E, Harenza JL, Molas S, Rais B, Anwar H, Zaveri NT, Maldonado R, Maskos U, McIntosh JM, Dierssen M, Miles MF, Chen X, De Biasi M, Damaj MI

Link to Pubmed [PMID] – 24750073

Br. J. Pharmacol. 2014 Aug;171(16):3845-57

BACKGROUND AND PURPOSE: Recent data have indicated that α3β4* neuronal nicotinic (n) ACh receptors may play a role in morphine dependence. Here we investigated if nACh receptors modulate morphine physical withdrawal.

EXPERIMENTAL APPROACHES: To assess the role of α3β4* nACh receptors in morphine withdrawal, we used a genetic correlation approach using publically available datasets within the GeneNetwork web resource, genetic knockout and pharmacological tools. Male and female European-American (n = 2772) and African-American (n = 1309) subjects from the Study of Addiction: Genetics and Environment dataset were assessed for possible associations of polymorphisms in the 15q25 gene cluster and opioid dependence.

KEY RESULTS: BXD recombinant mouse lines demonstrated an increased expression of α3, β4 and α5 nACh receptor mRNA in the forebrain and midbrain, which significantly correlated with increased defecation in mice undergoing morphine withdrawal. Mice overexpressing the gene cluster CHRNA5/A3/B4 exhibited increased somatic signs of withdrawal. Furthermore, α5 and β4 nACh receptor knockout mice expressed decreased somatic withdrawal signs compared with their wild-type counterparts. Moreover, selective α3β4* nACh receptor antagonists, α-conotoxin AuIB and AT-1001, attenuated somatic signs of morphine withdrawal in a dose-related manner. In addition, two human datasets revealed a protective role for variants in the CHRNA3 gene, which codes for the α3 nACh receptor subunit, in opioid dependence and withdrawal. In contrast, we found that the α4β2* nACh receptor subtype is not involved in morphine somatic withdrawal signs.

CONCLUSION AND IMPLICATIONS: Overall, our findings suggest an important role for the α3β4* nACh receptor subtype in morphine physical dependence.

http://www.ncbi.nlm.nih.gov/pubmed/24750073