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Ectopic galanin expression and normal galanin receptor 2 and galanin receptor 3 mRNA levels in the forebrain of galanin transgenic mice

Show simple item record Hohmann, John G. en_US Steiner, Robert A. en_US Perez, S. E. en_US Crawley, Jacqueline N. en_US Koprich, J. B. en_US Lipton, J. W. en_US Mufson, Elliott J. en_US He, B. en_US Counts, S. E. en_US 2008-10-17T20:42:06Z 2008-10-17T20:42:06Z 2005 en_US
dc.identifier.citation Neuroscience. 2005;133(2):371-80 en_US
dc.description.abstract The functional interactions of the neuropeptide galanin (GAL) occur through its binding to three G protein-coupled receptor subtypes: galanin receptor (GALR) 1, GALR2 and GALR3. Previously, we demonstrated that GALR1 mRNA expression was increased in the CA1 region of the hippocampus and discrete hypothalamic nuclei in galanin transgenic (GAL-tg) mice. This observation suggested a compensatory adjustment in cognate receptors in the face of chronic GAL exposure. To evaluate the molecular alterations to GALR2 and GALR3 in the forebrain of GAL overexpressing mice, we performed complementary quantitative, real-time PCR (qPCR), in situ hybridization, and immunohistochemistry in select forebrain regions of GAL-tg mice to characterize the neuronal distribution and magnitude of GAL mRNA and peptide expression and the consequences of genetically manipulating the neuropeptide GAL on the expression of GALR2 and GALR3 receptors. We found that GAL-tg mice displayed dramatic increases in GAL mRNA and peptide in the frontal cortex, posterior cortex, hippocampus, septal diagonal band complex, amygdala, piriform cortex, and olfactory bulb. Moreover, there was evidence for ectopic neuronal GAL expression in forebrain limbic regions that mediate cognitive and affective behaviors, including the piriform and entorhinal cortex and amygdala. Interestingly, regional qPCR analysis failed to reveal any changes in GALR2 or GALR3 expression in the GAL-tg mice, suggesting that, contrary to GALR1, these receptor genes are not under ligand-mediated regulatory control. The GAL-tg mouse model may provide a useful tool for the investigation of GAL ligand-receptor relationships and their role in normal cognitive and affective functions as well as in the onset of neurological disease. en_US
dc.language.iso en_US en_US
dc.publisher Elsevier en_US
dc.subject mouse en_US
dc.subject neuropeptides en_US
dc.subject galanin receptors en_US
dc.subject galaninergic en_US
dc.subject plasticity en_US
dc.subject.mesh Mice en_US
dc.subject.mesh Comparative Study en_US
dc.subject.mesh Galanin, genetics, metabolism en_US
dc.subject.mesh Mice, Transgenic en_US
dc.subject.mesh Immunohistochemistry, methods en_US
dc.subject.mesh In Situ Hybridization, methods en_US
dc.subject.mesh Receptor, Galanin, Type 3, genetics, metabolism en_US
dc.subject.mesh Research Support, N.I.H., Extramural en_US
dc.subject.mesh RNA, Messenger, metabolism en_US
dc.subject.mesh Reverse Transcriptase Polymerase Chain Reaction, methods en_US
dc.subject.mesh Prosencephalon, anatomy & histology, metabolism en_US
dc.subject.mesh Receptor, Galanin, Type 2, genetics, metabolism en_US
dc.subject.mesh Mice, Inbred C57BL en_US
dc.subject.mesh Animals en_US
dc.subject.mesh Research Support, U.S. Gov't, P.H.S. en_US
dc.subject.mesh Gene Expression Regulation, genetics en_US
dc.title Ectopic galanin expression and normal galanin receptor 2 and galanin receptor 3 mRNA levels in the forebrain of galanin transgenic mice en_US
dc.type Article en_US

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