Effects of haloperidol on CSF glutamate levels in drug-naive schizophrenic patients.

Dear Editors, It has recently been hypothesized that rather than an alteration in dopaminergic function, schizophrenia may arise as a consequence of an impaired function in excitatory amino acids (EAA j-mediated transmission (Kim et al., 1980). The evidence for this theory comes from (i) clinical data, although not replicated (Perry, T. L., 1982), in which low concentrations of glutamic acid (GLU) have been reported in the cerebrospinal fluid (CSF) of schizophrenic patients when compared to controls (Kim et al., 1980); (ii) binding studies in the brain of schizophrenic patients in which alterations in high-affinity [3H]-Kainate binding sites (Nishikawa et al., 1982; Kerwin et al., 1988) or [3H]-MK-801 binding sites (Kornhuber, et al.. 1989) in different brain areas have been reported; and (iii) the psychotomimetic effects of phencyclidine, a non-competitive antagonist of the N-methyl-D-aspartate (NMDA) receptor, which produces a paranoid syndrome that resembles schizophrenia or enhances psychotic symptoms in schizophrenic patients (Jaffe, 1985).