Literature DB >> 3325130

Evidence for differential regulation of corticotropin-releasing factor and vasopressin immunoreactivities in parvocellular neurosecretory and autonomic-related projections of the paraventricular nucleus.

P E Sawchenko1.   

Abstract

A combined retrograde transport-immunohistochemical method was used to compare the numbers of corticotropin-releasing factor (CRF) and vasopressin-immunoreactive neurons in the paraventricular nucleus of the hypothalamus (PVH) that could be retrogradely labeled after tracer injections in the dorsomedial medulla or the spinal cord in untreated, colchicine-treated, and adrenalectomized (ADX) male rats. In untreated animals, very few CRF-stained cells were retrogradely labeled after tracer injections in either target, while a modest number, comparable to that seen in previous studies, of vasopressinergic cells were found to project to one or both structures. Animals pretreated with colchicine, a non-specific inhibitor of axonal transport, displayed CRF immunoreactivity in a small percentage of retrogradely labeled neurons in the PVH; the number of retrogradely labeled vasopressin-immunoreactive cells was comparable to that seen in untreated rats. Despite the fact that ADX animals displayed enhanced immunostaining for both peptides in the parvocellular division of the PVH, the number of retrogradely labeled cells stained for each peptide was similar to that seen in controls. The results establish that CRF is contained within the long descending projections of the PVH, and are consistent with the view that adrenal steroid withdrawal preferentially enhances the expression of CRF and vasopressin in parvocellular neurosecretory neurons.

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Year:  1987        PMID: 3325130     DOI: 10.1016/0006-8993(87)91641-6

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


  29 in total

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Review 8.  Development of the neuroendocrine hypothalamus.

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9.  CRHR2 (Corticotropin-Releasing Hormone Receptor 2) in the Nucleus of the Solitary Tract Contributes to Intermittent Hypoxia-Induced Hypertension.

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