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Increase in [3H]cAMP binding sites and decrease in Gi alpha and Go alpha immunoreactivities in left temporal cortices

N Nishino1, N Kitamura, T Hashimoto

  • 1Department of Psychiatry and Neurology, Kobe University School of Medicine, Japan.

Brain Research
|June 25, 1993
PubMed
Summary
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Schizophrenia patients show increased cyclic adenosine monophosphate (cAMP) binding in the left temporal cortex, suggesting altered second messenger systems. Protein kinase C activity remained unchanged, indicating specific pathway involvement in the disease.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Psychiatry

Background:

  • Second messenger systems play crucial roles in neuronal function.
  • Alterations in these systems are implicated in the pathophysiology of schizophrenia.

Purpose of the Study:

  • To investigate potential changes in cyclic adenosine monophosphate (cAMP) and protein kinase C (PKC) signaling pathways in the temporal cortex (Brodmann's area 22) of schizophrenia patients.

Main Methods:

  • Measured [3H]cAMP and [3H]phorbol dibutyrate ([3H]PDBu) binding to assess protein kinase A and PKC activity, respectively.
  • Immunoquantified guanine nucleotide-binding proteins (G-proteins) using specific antisera.
  • Analyzed autopsy brain tissue from 10 schizophrenia patients and 10 age-matched controls.

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Main Results:

  • Significantly increased [3H]cAMP binding (approximately 30%) was observed in the soluble fraction of the left temporal cortex of schizophrenia patients compared to controls and the right hemisphere.
  • No significant differences in [3H]PDBu binding were found between schizophrenia patients and controls.
  • Specific [3H]cAMP binding sites were localized with the highest density in the cerebral cortex, hypothalamus, and amygdala.

Conclusions:

  • The findings suggest an upregulation of cAMP signaling in the left temporal cortex of individuals with schizophrenia.
  • This asymmetry in cAMP binding may indicate lateralized alterations in second messenger systems contributing to schizophrenia pathophysiology.
  • PKC signaling pathways appear unaffected in this cohort.