Analysis for mechanisms of neurotransmitter transport via Dysbindin

尽管精神疾病（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，谷氨酸或血清素功能障碍，神经发育障碍，怀孕期间的压力和病毒感染）。以有希望的危险因素为中心的分子通路的解剖，如精神分裂症中分裂- 1 (DISC1)，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，我发现了一种新的相互作用蛋白复合物，v - atp酶，作为DISC1的合作伙伴。我发现，与从野生型小鼠中分离的蛋白质相比，从disc1缺陷小鼠分离的突触囊泡中分离的v - atp酶亚基显著减少。

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.