1996
DOI: 10.1016/0006-8993(96)00041-8
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Distribution of c-Fos in guinea-pig brain following morphine withdrawal

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Cited by 17 publications
(9 citation statements)
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“…The Fos‐related antigen expression in control animals in the present experiments was higher than seen in previous experiments in which repeated subcutaneous injections of drugs were used (Chahl et al ., 1996). This might have been due to the stressful effect of repeated i.m.…”
Section: Discussioncontrasting
confidence: 80%
“…The Fos‐related antigen expression in control animals in the present experiments was higher than seen in previous experiments in which repeated subcutaneous injections of drugs were used (Chahl et al ., 1996). This might have been due to the stressful effect of repeated i.m.…”
Section: Discussioncontrasting
confidence: 80%
“…For example, this activating effect would possibly explain the c‐fos induction observed in the LC. Indeed, an increased expression of c‐fos mRNA during morphine withdrawal has been described in this structure which showed an intense expression of µ opiate receptors (Hayward et al ., 1990; Couceyro & Douglass, 1995; Chahl et al ., 1996). Alternatively, it is possible that other neurotransmitters, such as glutamate, mediate a part of the c‐fos mRNA induction in the LC, as previously shown in electrophysiological and behavioural studies (Rasmussen, 1995; Rasmussen et al ., 1996; Vandergriff & Rasmussen, 1999).…”
Section: Discussionmentioning
confidence: 99%
“…Investigation of the effects of stress‐related stimuli on the expression of the protein products of immediate‐early genes such as c‐fos is an effective means of evaluating the effects of a temporally defined stimulus on large populations of cells, with resolution of functional responses at the single‐cell level. Paradigms associated with increased anxiety or conditioned fear,30‐41 opiate withdrawal,42,43 and intracerebroventricular infusion of CRF or similar anxiogenic neuropeptides44,45 are effective at increasing immediate‐early gene expression within caudal regions of the DR. When these data are taken together with those indicating increased serotonergic neurotransmission in the DR in response to stressful stimuli,46,47 especially when the stressor is intense, uncontrollable, or unpredictable,48‐51 they suggest a mechanism whereby anxiogenic or fear‐inducing stimuli increase serotonergic neurotransmission via actions on subsets of serotonergic neurons within the caudal regions of the DR that give rise to a mesolimbocortical serotonergic innervation of the forebrain.…”
Section: Immediate‐early Gene Expression Studiesmentioning
confidence: 99%