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Distribution and regulation of galanin receptor 1 messenger RNA in the forebrain of wild type and galanin-transgenic mice

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dc.contributor.author Hohmann, John G. en_US
dc.contributor.author Jureus, Anders en_US
dc.contributor.author Teklemichael, Dawit N. en_US
dc.contributor.author Matsumoto, Alvin M. en_US
dc.contributor.author Clifton, Donald K. en_US
dc.contributor.author Steiner, Robert A. en_US
dc.date.accessioned 2008-10-17T20:42:33Z
dc.date.available 2008-10-17T20:42:33Z
dc.date.issued 2003 en_US
dc.identifier.citation Neuroscience. 2003;117(1):105-17 en_US
dc.identifier.uri http://hdl.handle.net/1773/4426
dc.description.abstract To learn more about molecular alterations in the brain that occur as a consequence of either the chronic excess or absence of peptide neurotransmitters, we examined the impact of genetically manipulating the neuropeptide galanin on the expression of one of its cognate receptors, galanin receptor 1. First, we examined the distribution of galanin receptor 1 messenger RNA in the mouse forebrain, and found it to be abundantly expressed in many brain regions, including in numerous hypothalamic and other forebrain regions associated with neuroendocrine function. The distribution of galanin receptor 1 messenger RNA in the mouse was similar to previous reports in the rat, with additional expression noted in the caudate putamen and in several midbrain regions. Next, using quantitative in situ hybridization, we measured cellular levels of galanin receptor 1 messenger RNA in the brains of mice that either overexpress galanin (galanin transgenic) or lack a functional galanin gene (galanin knockout). We report that relative to wild-type controls, the expression of galanin receptor 1 messenger RNA was increased in discrete areas of the brain in galanin-transgenic mice, but that depletion of galanin/noradrenergic innervation to the hypothalamus with the neurotoxin 6-hydroxydopamine did not alter levels of galanin receptor 1 messenger RNA. We also report that levels of galanin receptor 1 messenger RNA were not different between galanin-knockout and wild-type mice. These results suggest that compensatory adjustments in the expression of cognate receptors represent one mechanism by which the developing nervous system attempts to maintain homeostasis in response to overexpression of a peptidergic transmitter. However, the lack of significant changes in galanin receptor 1 messenger RNA in galanin-knockout mice suggests that developmentally programmed levels of receptor expression are maintained even in the complete absence of ligand. en_US
dc.language.iso en_US en_US
dc.publisher Endocrine Society en_US
dc.subject galanin en_US
dc.subject transgenic en_US
dc.subject receptor en_US
dc.subject knockout en_US
dc.subject hypothalamus en_US
dc.subject mouse en_US
dc.subject.mesh Mice, Knockout en_US
dc.subject.mesh Research Support, U.S. Gov't, P.H.S. en_US
dc.subject.mesh Male en_US
dc.subject.mesh Research Support, Non-U.S. Gov't en_US
dc.subject.mesh Research Support, U.S. Gov't, Non-P.H.S. en_US
dc.subject.mesh Animals en_US
dc.subject.mesh Comparative Study en_US
dc.subject.mesh Prosencephalon, chemistry, metabolism en_US
dc.subject.mesh Receptors, Galanin en_US
dc.subject.mesh Mice en_US
dc.subject.mesh Receptors, Neuropeptide, analysis, biosynthesis, deficiency, genetics en_US
dc.subject.mesh RNA, Messenger, analysis, biosynthesis en_US
dc.subject.mesh Mice, Transgenic en_US
dc.subject.mesh Mice, Inbred C57BL en_US
dc.title Distribution and regulation of galanin receptor 1 messenger RNA in the forebrain of wild type and galanin-transgenic mice en_US
dc.type Article en_US


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