Absence of basal ganglia amino acid neuron deficits in schizophrenia in three collections of brains.
Schizophr Res
; 31(2-3): 167-75, 1998 May 25.
Article
em En
| MEDLINE
| ID: mdl-9689721
ABSTRACT
Amino acid (glutamatergic, GABAergic) neuron deficiency theories of schizophrenia offer plausible explanations of pathogenesis. However, reports of disease-related reductions in amino acid synthesizing enzymes in post-mortem brains are contradictory. We measured neuronal uptake sites for gamma-aminobutyric acid (GABA; [3H]nipecotic acid binding) and nerve terminal/glial uptake sites for L-glutamate (D-[3H aspartate binding) in three independent groups of post-mortem brains from patients with schizophrenia and control subjects. Measurements were also made of the phencyclidine site of the glutamate N-methyl-D-aspartate (NMDA) receptor. Samples from patients showed no reductions in the binding of [3H]nipecotic acid or D-[3H]aspartate in caudate, putamen or globus pallidus. On the contrary, some increased binding of both ligands was observed in patients in many comparisons with controls. There were no clear-cut changes in NMDA receptor binding. The most consistent change in the brain sets was increased [3H]nipecotic acid binding in caudate-putamen. This could be due to neuroleptic treatment. The findings produce no evidence that schizophrenia involves major loss of GABA neuron terminals in the basal ganglia or losses of corticostriatal glutamatergic projections.
Buscar no Google
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas de Membrana Transportadoras
/
Esquizofrenia
/
Gânglios da Base
/
Prolina
/
Proteínas de Transporte
/
Transportadores de Cassetes de Ligação de ATP
/
Transportadores de Ânions Orgânicos
/
Proteínas de Membrana
Tipo de estudo:
Observational_studies
/
Risk_factors_studies
Limite:
Aged
/
Humans
/
Middle aged
Idioma:
En
Revista:
Schizophr Res
Assunto da revista:
PSIQUIATRIA
Ano de publicação:
1998
Tipo de documento:
Article
País de afiliação:
Reino Unido