dc.contributor.author | Hohmann, John G. | en_US |
dc.contributor.author | Steiner, Robert A. | en_US |
dc.contributor.author | Perez, S. E. | en_US |
dc.contributor.author | Crawley, Jacqueline N. | en_US |
dc.contributor.author | Koprich, J. B. | en_US |
dc.contributor.author | Lipton, J. W. | en_US |
dc.contributor.author | Mufson, Elliott J. | en_US |
dc.contributor.author | He, B. | en_US |
dc.contributor.author | Counts, S. E. | en_US |
dc.date.accessioned | 2008-10-17T20:42:06Z | |
dc.date.available | 2008-10-17T20:42:06Z | |
dc.date.issued | 2005 | en_US |
dc.identifier.citation | Neuroscience. 2005;133(2):371-80 | en_US |
dc.identifier.uri | http://hdl.handle.net/1773/4397 | |
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 |