Analysis for mechanisms of neurotransmitter transport via Dysbindin

虽然精神疾病（如精神分裂症）的病因机制在很大程度上仍然是深奥的，但已经提出了多种假设（例如多巴胺、谷氨酸或5-羟色胺功能障碍、神经发育障碍、妊娠期间的压力和病毒感染）。以有希望的风险因素为中心的分子途径的解剖，如分裂症1（DISC 1），可能有助于我们更好地了解这些疾病的发病机制。在这项研究中，我确定了一种新的相互作用的蛋白质复合物，V-ATP酶，作为DISC 1的伴侣。我发现，与从野生型小鼠分离的蛋白质相比，从DISC 1缺陷小鼠分离的突触囊泡组分中的几个V-ATP酶亚基的蛋白质显著减少。

Although the etiological mechanisms of psychiatric disorders, such as schizophrenia, remain largely esoteric, multiple hypotheses (e.g. dysfunction of dopamine, glutamate or serotonin, neurodevelopmental disorders, stress during pregnancy and viral infection) have been proposed. The dissection of molecular pathways centered on promising risk factors, such as Disrupted-In-Schizophrenia 1 (DISC1), may help us achieve a better understanding of the pathogenesis of these disorders. In this study, I identified a novel interacting protein complex, V-ATPase, as a partner of DISC1. I found significant protein reduction of a couple of V-ATPase subunits in synaptic vesicle fractions isolated from the DISC1-deficient mice compare to proteins isolated from the wildtype mice.