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Biol Psychiatry. 1998 Oct 15;44(8):667-74.

Glutamatergic neurotransmission involves structural and clinical deficits of schizophrenia.

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1
Laboratory of Molecular and Developmental Neuroscience, Harvard Medical School, Charlestown, Massachusetts, USA.

Abstract

BACKGROUND:

Phencyclidine and ketamine induce a syndrome closely resembling schizophrenia due to their blockade of N-methyl-D-aspartate (NMDA) receptor. These findings suggested that some aspects of schizophrenia are associated with decreased NMDA--glutamatergic function. We hypothesized that structural and symptomatic deficits in schizophrenia are related to glutamatergic neurotransmission.

METHODS:

We studied the relationships among cerebrospinal fluid (CSF) glutamatergic markers, clinical presentation of schizophrenia, and CT parameters of brain structure in drug-free schizophrenics.

RESULTS:

We found no significant differences between patients with schizophrenia and controls in CSF glutamatergic markers. When patients with schizophrenia were considered as a group, significant negative correlations between glutamatergic markers and brain structural measures as well as clinical measures were observed. Cluster analysis reveals a group of lower indices of glutamatergic neurotransmission, and more prominent thought disorder as well as ventricular enlargement, and a group with increased glutamate level.

CONCLUSIONS:

The findings support the hypothesis that altered glutamatergic neurotransmission plays a role in the brain structure and the clinical symptoms of schizophrenia.

PMID:
9798069
[Indexed for MEDLINE]
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