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Isotype-specific G protein abnormalities in the left superior temporal cortex and limbic structures of patients with
C Q Yang1, N Kitamura, N Nishino
1Department of Psychiatry and Neurology, Kobe University School of Medicine, Japan.
Background:
The potential role of signal transducing guanine nucleotide-binding regulatory protein (G protein) in schizophrenia is largely unknown.
Methods:
We immunoquantified isotypes of G protein using specific antisera against alpha and beta subunits of G protein in the superior temporal, prefrontal, and entorhinal cortices as well as the nucleus accumbens and amygdala of postmortem brains from 19 schizophrenic and 28 control subjects.
Results:
In the left hemisphere of schizophrenics, the amount of Gi alpha, Go alpha, and Gq alpha but not that of Gs alpha or G beta decreased in the superior temporal cortex by 27%, 27%, and 16%, respectively, as compared with the values in ipsilateral controls; the amount of any G protein isotype in the prefrontal and entorhinal cortices was not changed. In the nucleus accumbens and amygdala, the paranoid type schizophrenics showed a smaller amount of Gi alpha and Go alpha than the disorganized type schizophrenics. In the right superior temporal cortex, the isotype amount did not differ between the schizophrenic and control groups.
Conclusions:
The decreased Gq alpha immunoreactivity in the schizophrenic left superior temporal cortex may reflect the down-regulation of Gq alpha, resulting from chronic stimulation of Gq alpha-coupled receptors, while the decreased Gi alpha and Go alpha in the nucleus accumbens and amygdala of paranoid type schizophrenics may be related to the dopaminergic hyperactivity via dopamine D2 receptors.