Literature DB >> 8487952

Expression of c-fos in restricted areas of the basal forebrain and brainstem following single or combined intraventricular infusions of vasopressin and corticotropin-releasing factor.

L C Andreae1, J Herbert.   

Abstract

Vasopressin has been shown to be localized in specific central nervous system (CNS) sites. There is considerable evidence that it can act as a central neurotransmitter and it has been ascribed a variety of putative roles in the CNS. To identify those regions of the brain capable of responding to this peptide, 250 pmol vasopressin were infused into the lateral ventricle intracerebroventricular of conscious, handled male rats, and their brains processed for fos-immunohistochemistry 60 min later. Increases in fos-immunoreactivity, compared with cerebrospinal fluid-infused controls, were found in specific regions of the basal forebrain and brainstem: the central nucleus of the amygdala, ventrolateral septum, parvocellular divisions of the paraventricular nucleus of the hypothalamus, dorsal tuberal nucleus and locus coeruleus. Pre-infusion of 2500 pmol of a V1a antagonist prevented or reduced the expression of c-fos by intracerebroventricular vasopressin in all areas except the dorsal parvocellular paraventricular nucleus, implying that in most (but not all) areas the actions of vasopressin are mediated by the V1a receptor. Central administration of vasopressin had no effect on plasma corticosterone levels. Vasopressin and corticotropin-releasing factor act synergistically on the anterior pituitary to cause release of adrenocorticotropic releasing hormone and have corresponding synergistic interactions on behaviour. Infusion of 250 pmol corticotropin releasing factor produced a similar but not identical pattern of fos-like immunoreactivity to that of vasopressin. Activation of the parabrachial nucleus was observed, but there was no significant effect on the lateral septum and apparent increases in the medial parvocellular division of the paraventricular nucleus and locus coeruleus were not significant. Corticotropin releasing factor also caused a marked rise in plasma corticosterone. When the two peptides were infused together (125 pmol each) no evidence for synergy was found, in terms of the number of neurons activated to express c-fos. The induction of differential patterns of fos-like immunoreactivity by vasopressin and corticotropin-releasing factor in specific regions of the limbic forebrain and brainstem has implications for the individual roles they play in the CNS.

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Year:  1993        PMID: 8487952     DOI: 10.1016/0306-4522(93)90620-u

Source DB:  PubMed          Journal:  Neuroscience        ISSN: 0306-4522            Impact factor:   3.590


  4 in total

1.  Intranasal application of vasopressin fails to elicit changes in brain immediate early gene expression, neural activity and behavioural performance of rats.

Authors:  M Ludwig; V A Tobin; M F Callahan; E Papadaki; A Becker; M Engelmann; G Leng
Journal:  J Neuroendocrinol       Date:  2013-07       Impact factor: 3.627

2.  Do centrally administered neuropeptides access cognate receptors?: an analysis in the central corticotropin-releasing factor system.

Authors:  J C Bittencourt; P E Sawchenko
Journal:  J Neurosci       Date:  2000-02-01       Impact factor: 6.167

3.  Differential roles of amygdaloid nuclei in the anxiolytic- and antidepressant-like effects of the V1b receptor antagonist, SSR149415, in rats.

Authors:  N Salomé; J Stemmelin; C Cohen; G Griebel
Journal:  Psychopharmacology (Berl)       Date:  2006-06-02       Impact factor: 4.530

4.  Effect of serotonin depletion on the neuronal, endocrine and behavioural responses to corticotropin-releasing factor in the rat.

Authors:  Yasin Temel; Adel Helmy; Scarlett Pinnock; Joe Herbert
Journal:  Neurosci Lett       Date:  2003-02-27       Impact factor: 3.046

  4 in total

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