Interactions between developmental NMDA receptor dysfunction, genetic vulnerability and early-life stress in schizophrenia: studies of dysbindin mutant mice and living individuals at high risk of schizophrenia

本项目将研究涉及精神分裂症的两个关键途径：谷氨酸（兴奋性）神经传递和应激信号。我们将在一个精神分裂症相关的小鼠模型中研究谷氨酸能缺陷是如何在出生后的发育过程中出现的，在存在或不存在早期生活压力的情况下，并研究精神分裂症高风险个体的神经上皮细胞中应激和谷氨酸能缺陷之间的相互作用。

This project will investigate two key pathways implicated in schizophrenia: glutamatergic (excitatory) neurotransmission and stress signalling. We will study how glutamatergic deficits emerge across postnatal development, in the presence or absence of early-life stress, in a schizophrenia-relevant mouse model, and investigate the interactions between stress and glutamatergic deficits in neuroepithelial cells from living individuals at high risk of schizophrenia.