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The British Journal of Psychiatry (2000) 176: 236-242
© 2000 The Royal College of Psychiatrists

Synaptophysin gene expression in schizophrenia

Investigation of synaptic pathology in the cerebral cortex

SHARON L. EASTWOOD, DPhil and PAUL J. HARRISON, MRCPsych

University Departments of Psychiatry and Clinical Neurology (Neuropathology), Oxford

NIGEL J. CAIRNS, PhD

Department of Neuropathology, Institute of Psychiatry, London

Declaration of interest Work funded by grants to P.J.H. from the Wellcome Trust and Stanley Foundation. N.J.C. is supported by the Medical Research Council.

Correspondence: Dr P.J. Harrison, Neurosciences Building, University Department of Psychiatry, Warneford Hospital, Oxford OX37JX

Background Decreased expression of proteins such as synaptophysin in the hippocampus and prefrontal cortex in schizophrenia is suggestive of synaptic pathology. However, the overall profile of changes is unclear.

Aims To investigate synaptophysin gene expression in the cerebral cortex in schizophrenia.

Method The dorsolateral prefrontal (Brodmann area [BA] 9/46), anterior cingulate (BA 24), superior temporal (BA 22) and occipital (BA 17) cortex were studied in two series of brains, totalling 19 cases and 19 controls. Synaptophysin was measured by immunoautoradiography and immunoblotting. Synaptophysin messenger RNA (mRNA) was measured using in situ hybridisation.

Results Synaptophysin was unchanged in schizophrenia, except for a reduction in BA 17 of one brain series. Synaptophysin mRNA was decreased in BA17, and in BA 22 in the women with schizophrenia. No alterations were seen in BA 9/46.

Conclusions Synaptophysin expression is decreased in some cortical areas in schizophrenia. The alterations affect the mRNA more than the protein, and have an unexpected regional distribution. The characteristics of the implied synaptic pathology remain to be determined.




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