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Abnormal kainate receptor expression in prefrontal cortex in schizophrenia.

J H Meador-Woodruff¹, K L Davis, V Haroutunian

¹Mental Health Research Institute and Department of Psychiatry, University of Michigan, Ann Arbor, MI 48109-0720, USA. jimmw@umich.edu

Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology

|April 3, 2001

Summary

Schizophrenia involves glutamate synapse abnormalities. This study found altered kainate receptor expression, specifically changes in gluR7 and KA2 mRNA, in the prefrontal cortex of individuals with schizophrenia.

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Area of Science:

Neuroscience
Psychiatry
Molecular Biology

Background:

Glutamate synapse molecule abnormalities are linked to schizophrenia pathophysiology.
Ionotropic glutamate receptors (NMDA, AMPA, kainate) are implicated, but kainate receptors are less studied.

Purpose of the Study:

To investigate cortical and striatal kainate receptor expression in schizophrenia.
To compare expression levels in individuals with schizophrenia and a control group.

Main Methods:

In situ hybridization and receptor autoradiography were used on postmortem brain samples.
Examined subunit mRNA expression and receptor binding.

Main Results:

A shift in subunit stoichiometry (increased gluR7 mRNA, decreased KA2 mRNA) was observed in the prefrontal cortex.

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Reduced kainate receptor binding was found in specific layers of the prefrontal cortex in schizophrenia subjects.

No significant differences were noted in the striatum or occipital cortex.

Conclusions:

Kainate receptors are abnormally expressed in schizophrenia, particularly in the prefrontal cortex.
These findings support the role of ionotropic glutamate receptor disturbances in schizophrenia, extending beyond NMDA and AMPA receptors.