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c‐Fos and peptide immunoreactivities in the central extended amygdala of morphine‐dependent rats after naloxone‐precipitated withdrawal
Author(s) -
Veinante Pierre,
Stoeckel MarieElisabeth,
Lasbennes François,
FreundMercier MarieJosé
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02837.x
Subject(s) - stria terminalis , amygdala , extended amygdala , central nucleus of the amygdala , (+) naloxone , endocrinology , medicine , neuropeptide , c fos , neurochemical , morphine , central nervous system , chemistry , neuroscience , psychology , opioid , receptor , biochemistry , gene expression , gene
The central extended amygdala, a forebrain macrostructure, may represent a common substrate for acute drug reward and the dysphoric effects of drug withdrawal. To test its involvement during opiate withdrawal, we studied the distribution of c‐Fos immunoreactive neurons, in relation to their neuropeptide content, in brain sections from morphine‐dependent or naive rats, killed 90 min after naloxone or saline intraperitoneal injection. Naloxone treatment in naive rats induced a slight increase in c‐Fos immunoreactivity in the central amygdaloid nucleus, the lateral bed nucleus of the stria terminalis and the interstitial nucleus of the posterior limb of the anterior commissure. In morphine‐dependent rats, naloxone injection significantly increased the number of c‐Fos‐positive neurons in these structures as well as in the majority of the other central extended amygdala components. Double immunocytochemistry was used to determine the neurochemical nature of c‐Fos‐positive neurons in the central extended amygdala. Corticotropin‐releasing factor‐ and methionine‐enkephakin‐immunoreactive neurons displayed c‐Fos immunoreactivity in naive rats after naloxone injection, whereas only enkephalinergic neurons were found to be c‐Fos positive in morphine‐dependent rats after naloxone injection. The possible involvement of the corticotropin‐releasing factor system during withdrawal is discussed. These results suggest that the whole central extended amygdala is activated during opiate withdrawal, with a lateral to medial decreasing gradient, and emphasize the role of peptidergic systems in this morphofunctional continuum.

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