| Regional and subtype selective changes of neurotransmitter receptor density in a rat transgenic for the Huntington's disease mutation. | |
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MedLine Citation:
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PMID: 16033418 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Huntington's disease (HD) is an autosomal dominantly inherited progressive neurodegenerative disorder caused by a CAG/polyglutamine repeat expansion in the gene encoding the huntingtin protein. We have recently generated a rat model transgenic for HD, which displays a slowly progressive phenotype resembling the human adult-onset type of disease. In this study we systematically assessed the distribution and density of 17 transmitter receptors in the brains of 2-year-old rats using quantitative multi-tracer autoradiography and high-resolution positron emission tomography. Heterozygous animals expressed increased densities of M(2) acetylcholine (increase of 148 +/- 16% of controls; p > 0.001; n = 7), nicotine (increase of 149 +/- 16% of controls; p > 0.01; n = 6), and alpha(2) noradrenergic receptors (increase of 141 +/- 15% of controls; p > 0.001; n = 6), respectively. Densities of these receptors were decreased in homozygous animals. Decreases of receptor density in both hetero- and homozygous animals were found for M1 acetylcholine, 5-HT 2A serotonin, A 2A adenosine, D1 and D2 dopamine, and GABA(A) receptors, respectively. Other investigated receptor systems showed small changes or were not affected. The present data suggest that the moderate increase of CAG/polyglutamine repeat expansions in the present rat model of Huntington's disease is characterized by subtype-selective and region-specific changes of neuroreceptor densities. In particular, there is evidence for a contribution of predominantly presynaptically localized cholinergic and noradrenergic receptors in the response to Huntington's disease pathology. |
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Authors:
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Andreas Bauer; Karl Zilles; Andreas Matusch; Carsten Holzmann; Olaf Riess; Stephan von Hörsten |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of neurochemistry Volume: 94 ISSN: 0022-3042 ISO Abbreviation: J. Neurochem. Publication Date: 2005 Aug |
Date Detail:
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Created Date: 2005-07-21 Completed Date: 2005-09-19 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 2985190R Medline TA: J Neurochem Country: England |
Other Details:
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Languages: eng Pagination: 639-50 Citation Subset: IM |
Affiliation:
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Institute of Medicine, Research Center Jülich, Jülich, Germany. an.bauer@fz-juelich.de |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Animals, Genetically Modified Autoradiography / methods Brain / anatomy & histology, metabolism*, radionuclide imaging Brain Mapping Disease Models, Animal Huntington Disease / genetics* Image Processing, Computer-Assisted / methods Mutation Positron-Emission Tomography / methods Radioligand Assay / methods Rats Receptors, Neurotransmitter / classification, metabolism* Time Factors Trinucleotide Repeat Expansion / genetics* |
| Chemical | |
Reg. No./Substance:
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0/Receptors, Neurotransmitter |
| Comments/Corrections | |
Erratum In:
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J Neurochem. 2005 Aug;94(4):1167 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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