Evidence of glutamatergic deficiency in schizophrenia

Studies of amino acid release were carried out using frozen sections from brains of schizophrenics and controls. Synaptosomes were prepared via differential centrifugation in Ficoll allowing the veratridine-induced release of aspartate, glutamate, glycine, and GABA to be measured. The release of glu...

Full description

Saved in:
Bibliographic Details
Published inNeuroscience letters Vol. 121; no. 1-2; p. 77
Main Authors Sherman, A D, Davidson, A T, Baruah, S, Hegwood, T S, Waziri, R
Format Journal Article
LanguageEnglish
Published Ireland 02.01.1991
Subjects
Aged
Aspartic Acid - metabolism
Brain Chemistry
Cerebral Cortex - chemistry
Cerebral Cortex - metabolism
Female
gamma-Aminobutyric Acid - metabolism
Glutamate Decarboxylase - metabolism
Glutamates - deficiency
Glutamic Acid
Haloperidol
Humans
In Vitro Techniques
Male
Middle Aged
Schizophrenia - metabolism
Synaptosomes - chemistry
Synaptosomes - metabolism
Veratridine
Online AccessGet more information

Cover

More Information
Summary:Studies of amino acid release were carried out using frozen sections from brains of schizophrenics and controls. Synaptosomes were prepared via differential centrifugation in Ficoll allowing the veratridine-induced release of aspartate, glutamate, glycine, and GABA to be measured. The release of glutamate and gamma-aminobutyric acid (GABA) was reduced in the synaptosomes from schizophrenics. This decrease could be reversed partially by pre-incubation of the synaptosomes with haloperidol. Additionally, the activity of glutamate decarboxylase was decreased and partially restored by haloperidol pre-incubation. These data are consistent with the hypothesis of a glutamatergic/GABAergic deficit in schizophrenia.
ISSN:0304-3940
DOI:10.1016/0304-3940(91)90653-B