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dc.contributor.authorHohmann, John G.en_US
dc.contributor.authorSteiner, Robert A.en_US
dc.contributor.authorPerez, S. E.en_US
dc.contributor.authorCrawley, Jacqueline N.en_US
dc.contributor.authorKoprich, J. B.en_US
dc.contributor.authorLipton, J. W.en_US
dc.contributor.authorMufson, Elliott J.en_US
dc.contributor.authorHe, B.en_US
dc.contributor.authorCounts, S. E.en_US
dc.date.accessioned2008-10-17T20:42:06Z
dc.date.available2008-10-17T20:42:06Z
dc.date.issued2005en_US
dc.identifier.citationNeuroscience. 2005;133(2):371-80en_US
dc.identifier.urihttp://hdl.handle.net/1773/4397
dc.description.abstractThe 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.isoen_USen_US
dc.publisherElsevieren_US
dc.subjectmouseen_US
dc.subjectneuropeptidesen_US
dc.subjectgalanin receptorsen_US
dc.subjectgalaninergicen_US
dc.subjectplasticityen_US
dc.subject.meshMiceen_US
dc.subject.meshComparative Studyen_US
dc.subject.meshGalanin, genetics, metabolismen_US
dc.subject.meshMice, Transgenicen_US
dc.subject.meshImmunohistochemistry, methodsen_US
dc.subject.meshIn Situ Hybridization, methodsen_US
dc.subject.meshReceptor, Galanin, Type 3, genetics, metabolismen_US
dc.subject.meshResearch Support, N.I.H., Extramuralen_US
dc.subject.meshRNA, Messenger, metabolismen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reaction, methodsen_US
dc.subject.meshProsencephalon, anatomy & histology, metabolismen_US
dc.subject.meshReceptor, Galanin, Type 2, genetics, metabolismen_US
dc.subject.meshMice, Inbred C57BLen_US
dc.subject.meshAnimalsen_US
dc.subject.meshResearch Support, U.S. Gov't, P.H.S.en_US
dc.subject.meshGene Expression Regulation, geneticsen_US
dc.titleEctopic galanin expression and normal galanin receptor 2 and galanin receptor 3 mRNA levels in the forebrain of galanin transgenic miceen_US
dc.typeArticleen_US


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