Cingulate cortex synaptic terminal proteins and neural cell adhesion molecule in schizophrenia

Cingulate cortex synaptic terminal proteins and neural cell adhesion molecule in schizophrenia
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DOI:
10.1016/s0306-4522(96)00489-7
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发表时间:
1997-05-01
期刊:
影响因子:
3.3
通讯作者:
Trimble, WS
Trimble, WS
中科院分区:
医学3区
文献类型:
--
作者:
Honer, WG;Falkai, P;Trimble, WS

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精神分裂症患者扣带皮层的神经元组织和传入神经支配模式异常,并且可能存在突触末梢的相关变化。通过生化和融合蛋白研究将一组单克隆抗体定义为检测突触蛋白(抗体 SP6)、突触素(抗体 SP4)和突触体相关蛋白 25(抗体 SP12)。这些抗体和与神经细胞粘附分子反应的多克隆抗体被用来研究精神分裂症的扣带皮层。免疫细胞化学表明突触蛋白免疫反应性的分布比突触素的分布要广得多。总体而言,多变量分析表明,与对照组相比,精神分裂症患者的突触末端蛋白免疫反应性有所增加(P=0.004)。控制年龄和死后间隔后,精神分裂症患者突触蛋白免疫反应性显着升高(P=0.004),神经细胞粘附分子免疫反应性也升高(P=0.05)。神经细胞粘附分子与突触素比值升高(P=0.005),可能表明精神分裂症存在较不成熟的突触。突触蛋白免疫反应性升高与精神分裂症扣带皮层谷氨酸传入神经增加一致,结合神经细胞粘附分子与突触素比值结果提示精神分裂症该区域突触功能可能存在异常。 (C) 1997 国际广播组织。
The neuronal organization and patterns of afferent innervation are abnormal in the cingulate cortex in schizophrenia, and associated changes in synaptic terminals could be present. A panel of monoclonal antibodies was defined with biochemical and fusion protein studies as detecting syntaxin (antibody SP6), synaptophysin (antibody SP4) and synaptosomal-associated protein-25 (antibody SP12). These antibodies and a polyclonal antibody reactive with neural cell adhesion molecule were used to investigate the cingulate cortex in schizophrenia. Immunocytochemistry indicated that syntaxin immunoreactivity had a considerably wider distribution than synaptophysin. Overall, multivariate analysis indicated increased synaptic terminal protein immunoreactivity in schizophrenia compared to controls (P=0.004). Controlled for age and post mortem interval, syntaxin immunoreactivity was significantly elevated in schizophrenia (P=0.004), and neural cell adhesion molecule immunoreactivity was also elevated (P=0.05). The neural cell adhesion molecule to synaptophysin ratio was increased (P=0.005), possibly indicating the presence of less mature synapses in schizophrenia.Elevated syntaxin immunoreactivity is consistent with increased glutamatergic afferents to the cingulate cortex in schizophrenia, and combined with the neural cell adhesion molecule to synaptophysin ratio results suggests that synaptic function in this region in schizophrenia may be abnormal. (C) 1997 IBRO.