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  • Original Research Article
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Reduction of synapsin in the hippocampus of patients with bipolar disorder and schizophrenia

Abstract

Several studies suggest that decreased expression of presynaptic proteins may be characteristic of schizophrenia. We examined one such protein, synapsin, in schizophrenia and bipolar disorder. Samples of hippocampal tissue from controls (n = 13), patients with schizophrenia (n = 16), or bipolar disorder (n = 6), and suicide victims (n = 7) were used. The membrane and cytosolic fractions were analyzed by Western immunoblotting for synapsin using an antibody that detects synapsin Ia, IIa, and IIIa proteins. Synaptophysin was also measured for comparison. Total synapsin was decreased significantly in patients with schizophrenia (P = 0.034) and in bipolar disorder (P = 0.00008) as compared to controls. The synapsin/synaptophysin ratios were decreased in schizophrenia and bipolar disorder, and additionally in suicide victims (P = 0.014). Age, postmortem interval, percentage of protein extracted, and pH of brain were not different between groups. No changes in total synapsin or synaptophysin in the hippocampus were produced by injecting rats with either lithium or haloperidol for 30 days. Reductions in synapsin in both patients with schizophrenia (synapsin IIa and IIIa) and bipolar disorder (synapsin Ia, IIa and IIIa) imply that altered or reduced synaptic function in the hippocampus may be involved in these disorders.

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Acknowledgements

We wish to thank Bruce Ladenheim for dissection of hippocampus from rat brain and Drs HT Kao and Paul Greengard, Rockefeller University, for synapsin antibody G304, and additional immunoblots. Dr Mary Herman, Clinical Brain Disorders Branch, NIMH, Bethesda, MD assisted with providing the human hippocampus samples used in this study. Generous support was received from the William Lion Penzner Foundation (MPV).

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Correspondence to W J Freed.

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Vawter, M., Thatcher, L., Usen, N. et al. Reduction of synapsin in the hippocampus of patients with bipolar disorder and schizophrenia. Mol Psychiatry 7, 571–578 (2002). https://doi.org/10.1038/sj.mp.4001158

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