This is the authors' abstract. We don't add key points for this paper.
OBJECTIVE: The purpose of this study was to test the hypothesis that abnormalities in the parvalbumin-containing subclass of local circuit neurons contribute to altered gamma-aminobutyric acid (GABA) neurotransmission in the prefrontal cortex of schizophrenic subjects. METHOD: Profile counts and somal size measures were made of parvalbumin-immunoreactive neurons in areas 9, 46, and 17 from 15 matched pairs of schizophrenic and normal comparison subjects. RESULTS: No differences in relative density, laminar distribution, or somal size of labeled neurons were found in any region. CONCLUSIONS: These findings suggest that altered GABA neurotransmission in schizophrenia is due to either abnormalities in other sub-populations of prefrontal cortical GABA neurons or abnormalities in the parvalbumin-containing subclass that could not be detected in the present study.
No takes yet. Share an insight, caveat, or question.
Woo et al. (1997) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: