Document Detail


Amino acid neurotransmitter abnormalities in Huntington's disease and the quinolinic acid animal model of Huntington's disease.
MedLine Citation:
PMID:  2892568     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Concentrations of gamma-aminobutyric acid (GABA), glutamate, aspartate, and taurine were measured in postmortem tissue from the brains of patients with Huntington's disease (HD) and in the quinolinic acid (QA) lesioned rat striatum. The aim of the study was to assess further the ability of the QA model of HD to reproduce the neurochemical features of the disease. Nine cortical and 9 subcortical regions were examined from 17 pathologically graded cases of HD and 10 controls. Significant reductions in both GABA and glutamate were found in HD striatum. The reductions were greater in the more severely affected grades of HD, and there was a gradient of amino acid loss across the striatal nuclei (caudate greater than putamen greater than nucleus accumbens) which was consistent with the known pattern of pathological involvement. Taurine and aspartate concentrations showed no significant change. GABA reductions were found in both segments of the globus pallidus (external greater than internal) and both parts of the substantia nigra (reticulata greater than compacta). In advanced cases of HD, there were significant reductions in glutamate in Brodmann cortical areas 3-1-2, 6, 9, and 17, but GABA, aspartate, and taurine were unaltered in the cortex. The QA lesions reproduced the striatal deficits of both GABA and glutamate but, in contrast to HD, there was a decrease in taurine, possibly due to species differences. Chronic QA lesions resulted in a secondary dying back of corticostriatal glutamatergic terminals, but did not produce a change in cortical glutamate concentration. This suggests that reductions in cortical glutamate in HD may reflect a primary loss of glutamatergic neurons. Our findings extend previous observations on amino acid neurotransmitters in HD and, with the exception of taurine, confirm the general applicability of the QA model.
Authors:
D W Ellison; M F Beal; M F Mazurek; J R Malloy; E D Bird; J B Martin
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Brain : a journal of neurology     Volume:  110 ( Pt 6)     ISSN:  0006-8950     ISO Abbreviation:  Brain     Publication Date:  1987 Dec 
Date Detail:
Created Date:  1988-03-07     Completed Date:  1988-03-07     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0372537     Medline TA:  Brain     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  1657-73     Citation Subset:  AIM; IM    
Affiliation:
Department of Neurology, Massachusetts General Hospital, Boston 02114.
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MeSH Terms
Descriptor/Qualifier:
Amino Acids / metabolism*
Animals
Brain / metabolism
Decerebrate State
Humans
Huntington Disease / chemically induced,  metabolism*
Neurotransmitter Agents / metabolism*
Quinolinic Acid
Quinolinic Acids
Rats
Tissue Distribution
Grant Support
ID/Acronym/Agency:
IR23NS19867-1/NS/NINDS NIH HHS; MNINS 31862/NS/NINDS NIH HHS; NS 16367/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Amino Acids; 0/Neurotransmitter Agents; 0/Quinolinic Acids; 89-00-9/Quinolinic Acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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