Reactivity and plasticity in the amygdala nuclei during opiate withdrawal conditioning: Differential expression of c-fos and arc immediate early genes

M. Lucas, F. Frenois, C. Vouillac, L. Stinus, M. Cador, C. Le Moine
Neuroscience. 2008-06-01; 154(3): 1021-1033
DOI: 10.1016/j.neuroscience.2008.04.006

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1. Neuroscience. 2008 Jun 26;154(3):1021-33. doi:
10.1016/j.neuroscience.2008.04.006. Epub 2008 Apr 11.

Reactivity and plasticity in the amygdala nuclei during opiate withdrawal
conditioning: differential expression of c-fos and arc immediate early genes.

Lucas M(1), Frenois F, Vouillac C, Stinus L, Cador M, Le Moine C.

Author information:
(1)Université Victor Segalen Bordeaux 2, Université Bordeaux 1, CNRS UMR 5227,
Team « Neuropsychopharmacology of Addiction, » 146 bis rue Léo Saignat, 33076
Bordeaux, France.

Opiate withdrawal leads to the emergence of an aversive state that can be
conditioned to a specific environment. Reactivation of these withdrawal memories
has been suggested to be involved in relapse to drug-seeking of abstinent opiate
addicts. Among the limbic areas that are likely to mediate these features of
opiate dependence, amygdala nuclei represent critical neural substrates. Using a
conditioned place aversion paradigm (CPA), we have previously shown specific
opposite patterns of reactivity in the basolateral (BLA) and the central (CeA)
amygdala, when comparing the experience of acute opiate withdrawal with the
re-exposure to a withdrawal-paired environment. These data gave clues about the
potential mechanisms by which amygdala nuclei may be involved in withdrawal
memories. To extend these results, the present study aimed to assess the cellular
reactivity and plasticity of amygdala nuclei during the opiate withdrawal
conditioning process. For this, we have quantified c-fos and arc expression using
in situ hybridization in rats, following each of the three conditioning sessions
during CPA, and after re-exposure to the withdrawal-paired environment. BLA
output neurons showed an increase in the expression of the plasticity-related arc
gene during conditioning that was also increased by re-exposure to the
withdrawal-paired environment. Interestingly, the CeA showed an opposite pattern
of responding, and the intercalated cell masses (ITC), a possible inhibitory
interface between the BLA and CeA, showed a persistent activation of c-fos and
arc mRNA. We report here specific c-fos and arc patterns of reactivity in
amygdala nuclei during withdrawal conditioning. These findings improve our
understanding of the involvement of the amygdala network in the formation and
retrieval of withdrawal memories. Plasticity processes within BLA output neurons
during conditioning, may participate in increasing the BLA reactivity to
conditioned stimuli, which could in turn (by the control of downstream nuclei)
reinforce and drive the motivational properties of withdrawal over drug

DOI: 10.1016/j.neuroscience.2008.04.006
PMID: 18501523 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus