Reduction of synapsin in the hippocampus of patients with bipolar disorder and schizophrenia

被引:159
作者
Vawter, MP
Thatcher, L
Usen, N
Hyde, TM
Kleinman, JE
Freed, WJ
机构
[1] NIDA, Cellular Neurobiol Branch, IRP, Baltimore, MD 21224 USA
[2] NIMH, Clin Brain Disorders Branch, NIH, Bethesda, MD 20892 USA
[3] Univ Calif Irvine, Irvine, CA USA
关键词
synaptophysin; synapsin; schizophrenia; bipolar disorder; mood disorder; hippocampus;
D O I
10.1038/sj.mp.4001158
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 to = 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 la, 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.
引用
收藏
页码:571 / 578
页数:8
相关论文
共 46 条
[41]   Alterations of hippocampal secreted N-CAM in bipolar disorder and synaptophysin in schizophrenia [J].
Vawter, MP ;
Howard, AL ;
Hyde, TM ;
Kleinman, JE ;
Freed, WJ .
MOLECULAR PSYCHIATRY, 1999, 4 (05) :467-475
[42]   SYNAPSIN-IA, SYNAPSIN-IB, PROTEIN-IIIA, AND PROTEIN-IIIB, 4 RELATED SYNAPTIC VESICLE-ASSOCIATED PHOSPHOPROTEINS, SHARE REGIONAL AND CELLULAR-LOCALIZATION IN RAT-BRAIN [J].
WALAAS, SI ;
BROWNING, MD ;
GREENGARD, P .
JOURNAL OF NEUROCHEMISTRY, 1988, 51 (04) :1214-1220
[43]   IMPLICATIONS OF NORMAL BRAIN-DEVELOPMENT FOR THE PATHOGENESIS OF SCHIZOPHRENIA [J].
WEINBERGER, DR .
ARCHIVES OF GENERAL PSYCHIATRY, 1987, 44 (07) :660-669
[44]   Transcription of actin, cyclophilin and glyceraldehyde phosphate dehydrogenase genes: tissue- and treatment-specificity [J].
Weisinger, G ;
Gavish, M ;
Mazurika, C ;
Zinder, O .
BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION, 1999, 1446 (03) :225-232
[45]   SCHIZOPHRENIA - GENETICS AND THE MATERNAL IMMUNE-RESPONSE TO VIRAL-INFECTION [J].
WRIGHT, P ;
GILL, M ;
MURRAY, RM .
AMERICAN JOURNAL OF MEDICAL GENETICS, 1993, 48 (01) :40-46
[46]   SNAP-25 deficit and hippocampal connectivity in schizophrenia [J].
Young, CE ;
Arima, K ;
Xie, J ;
Hu, L ;
Beach, TG ;
Falkai, P ;
Honer, WG .
CEREBRAL CORTEX, 1998, 8 (03) :261-268