兴奋性-抑制性神经活动失衡在自闭症谱系障碍（Autism Spectrum Disorder，ASD）的病理发生中起着重要作用。最近研究发现，Tripartie motif (TRIM) 32，一种E3泛素连接酶，与ASD有高度基因相关性。我们前期结果显示， TRIM32-/-小鼠表现出社交障碍和重复性行为这些类似ASD的行为，说明TRIM32是ASD的危险基因。TRIM32在神经前体细胞上高表达。TRIM32-/-小鼠皮层第VI层锥体神经元数量和parvalbumin+中间神经元数量明显减少，说明TRIM32可能调控谷氨酸能锥体神经元和GABA能中间神经元的产生。因此，本课题拟利用TRIM32-/-小鼠，研究TRIM32在谷氨酸能锥体神经元和GABA能中间神经元的产生中的作用和机制，分析其对兴奋性-抑制性神经活动平衡的影响，从而阐述TRIM32在ASD病理发生中的作用机制。

An imbalance between excitatory-inhibitory neurotransmission is suggested involved in the pathogenesis of autism spectrum disorder (ASD), a developmental neuropsychiatric disease. Previous studies indicate that deletion of tripartie motif 32 (TRIM32) gene is associated with ASD. Our preliminary data show TRIM32-/- mice exhibit impaired social interaction and repetitive behaviors in three chamber social preference test and self-grooming test, respectively, suggesting a potential function of TRIM32 in ASD pathology. TRIM32 is highly expressed in neural progenitor cells locating in the dorsal subventricular zone and the medial ganglionic emience, where pyramidal neurons and GABAergic interneurons arise. Decreased numbers of layer VI cortical neurons and parvalbumin+ interneurons have been observed in TRIM32-/- mice，suggesting a potential function of TRIM32 in generation of glutamatergic pyramidal neurons and GABAergic interneurons.Therefore, in this project, we will clarify the function of TRIM32 in the pathogenesis of ASD by investigating its role in the generation of glutamatergic pyramidal neurons and GABAergic interneuron in the developing cerebral cortex, and thus in maintenance of inhibitory-excitatory balance of neural circuitry.