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Titolo:
Abnormalities in the synaptic vesicle fusion machinery in Huntington's disease
Autore:
Morton, AJ; Faull, RLM; Edwardson, JM;
Indirizzi:
Univ Cambridge, Dept Pharmacol, Cambridge CB2 1QJ, England Univ CambridgeCambridge England CB2 1QJ col, Cambridge CB2 1QJ, England Univ Auckland, Fac Med & Hlth Sci, Dept Anat, Auckland 1, New Zealand UnivAuckland Auckland New Zealand 1 Dept Anat, Auckland 1, New Zealand
Titolo Testata:
BRAIN RESEARCH BULLETIN
fascicolo: 2, volume: 56, anno: 2001,
pagine: 111 - 117
SICI:
0361-9230(20010915)56:2<111:AITSVF>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
NEUROTRANSMITTER RELEASE; MEMBRANE-FUSION; PROTEIN; MICE; RAB3A; BRAIN; INVOLVEMENT; EXOCYTOSIS; COMPLEXINS; MUTATION;
Keywords:
Huntington's disease; complexin II; striosome; matrix; SNARE; human; neurodegeneration;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Morton, AJ Univ Cambridge, Dept Pharmacol, Tennis Court Rd, Cambridge CB2 1QJ, England Univ Cambridge Tennis Court Rd Cambridge England CB2 1QJ gland
Citazione:
A.J. Morton et al., "Abnormalities in the synaptic vesicle fusion machinery in Huntington's disease", BRAIN RES B, 56(2), 2001, pp. 111-117

Abstract

We have recently described the progressive and selective loss of the presynaptic protein complexin II in brains of mice (R6/2) transgenic for the Huntington's disease (HD) mutation. Here we have determined the expression of components of the synaptic vesicle fusion machinery in the striatum and hippocampus from post-mortem brains of HD cases and neurologically normal controls. As in the brains of R6/2 mice, complexin II was markedly depleted in the HD striatum; the depletion was compartmentally organized, with complexin II-poor regions corresponding with areas of low immunoreactivity toward the matrix marker calbindin D-28K. Decreases in the levels of the soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptor (SNARE)protein synaptobrevin 2 and of rab3A were also seen, but none of the otherproteins tested was significantly affected. In the hippocampus, levels of complexin II, synaptobrevin 2, rab3A, and also of alpha -SNAP, were markedly elevated in HD brains. We suggest that the observed abnormalities in the expression of proteins known to be involved in the control of neurotransmitter release, including both modulators and core components of the vesicle fusion machinery, might account for at least some of the functional abnormalities seen in HD. (C) 2001 Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/21 alle ore 03:37:09