Synaptic plasticity is the neural basis of physiological processes involved in learning and memory. Tripartite motif-containing 32 (TRIM32) has been found to play many important roles in the brain such as neural stem cell proliferation, neurogenesis, inhibition of nerve proliferation, and apoptosis. TRIM32 has been linked to several nervous system diseases including autism spectrum disorder, depression, anxiety, and Alzheimer’s disease. However, the role of TRIM32 in regulating the mechanism of synaptic plasticity is still unknown. Our electrophysiological studies using hippocampal slices revealed that long-term potentiation of CA1 synapses was impaired in TRIM32 deficient (KO) mice. Further research found that dendritic spines density, AMPA receptors, and synaptic plasticity-related proteins were also reduced. NMDA receptors were upregulated whereas GABA receptors were downregulated in TRIM32 deficient mice, explaining the imbalance in excitatory and inhibitory neurotransmission. This caused overexcitation leading to decreased neuronal numbers in the hippocampus and cortex. In summary, this study provides this maiden evidence on the synaptic plasticity changes of TRIM32 deficiency in the brain and proposes that TRIM32 relates the notch signaling pathway and its related mechanisms contribute to this deficit.

中文翻译：

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TRIM32 缺陷通过 Notch 通路通过兴奋性-抑制性失衡损害突触可塑性。

突触可塑性是参与学习和记忆的生理过程的神经基础。已发现含有三联基序的 32 (TRIM32) 在大脑中发挥许多重要作用，例如神经干细胞增殖、神经发生、抑制神经增殖和细胞凋亡。TRIM32 与多种神经系统疾病有关，包括自闭症谱系障碍、抑郁、焦虑和阿尔茨海默病。然而，TRIM32在调节突触可塑性机制中的作用仍不清楚。我们使用海马切片的电生理学研究表明，在 TRIM32 缺陷 (KO) 小鼠中，CA1 突触的长期增强功能受损。进一步的研究发现，树突棘密度、AMPA 受体和突触可塑性相关蛋白也降低了。NMDA 受体上调而 GABA 受体在 TRIM32 缺陷小鼠中下调，解释了兴奋性和抑制性神经传递的不平衡。这导致过度兴奋，导致海马体和皮质中的神经元数量减少。总之，这项研究提供了关于大脑中 TRIM32 缺陷的突触可塑性变化的首次证据，并提出 TRIM32 与缺口信号通路及其相关机制有关。