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 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.
Sherman
A D
AD
University of Iowa, Department of Psychiatry, Iowa City 52242.
Davidson
A T
AT
Baruah
S
S
Hegwood
T S
TS
Waziri
R
R
D000368:Aged; D001224:Aspartic Acid / Q000378:metabolism; D001923:Brain Chemistry; D002540:Cerebral Cortex / Q000737:chemistry / Q000378:metabolism; D005260:Female; D005968:Glutamate Decarboxylase / Q000378:metabolism; D005971:Glutamates / Q000172:deficiency*; D018698:Glutamic Acid; D006220:Haloperidol; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D008875:Middle Aged; D012559:Schizophrenia / Q000378:metabolism*; D013574:Synaptosomes / Q000737:chemistry / Q000378:metabolism; D014701:Veratridine; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D005971:Glutamates; D001224:Aspartic Acid; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D014701:Veratridine; D005968:Glutamate Decarboxylase; D006220:Haloperidol