Abstract

Galanin (GAL) is a 29-amino acid peptide that is present in the hypothalamic magnocellular neurons of the rat supraoptic nucleus (SON) and paraventricular nucleus (PVN). Since previous studies revealed a possible role of GAL in the hydro-osmotic regulation, we have investigated the effects of GAL on the vasopressin (AVP) mRNA content in the hypothalamic magnocellular neurons. We demonstrated by in situ hybridization (ISH) and immunohistochemistry that 100 pmol of GAL or GAL fragment (1-16) injected into the lateral ventricle of anesthetized dehydrated male rats induced a rapid (10 min time interval) decrease of AVP mRNA and AVP content in the magnocellular cell bodies of SON and PVN. These effects were quantified on an autoradiographic film and were also obvious at the cellular level by using ISH with a radiolabeled or digoxigenin-labeled oligonucleotide probe. Oxytocin mRNA content is not altered by the same injection either in dehydrated male or lactating female rats. Under the same conditions of lactation, AVP mRNA content is not modified and the i.c.v. injection of GAL has no effect. GAL antagonist (M15) injection suppressed the GAL-induced decrease of AVP mRNA in the dehydrated rats and increased AVP mRNA level in control rats. The efficacy of M15 in antagonizing GAL effects on AVP mRNA suggests the involvement of GAL receptors in the regulation of the vasopressinergic cell bodies. Moreover, endogenous GAL seems to depress the AVP mRNA content of SON and PVN in vivo. The possible origin of endogenous GAL and the mechanisms by which GAL can regulate the AVP mRNA content are also discussed.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.