Investigation of synaptic maintenance mechanisms via inositol trisphosphate signaling in neurons and glial cells

为了保证大脑信息处理的稳定，突触功能必须得到维持。人们认识到，经验输入的关闭会导致相应大脑功能的衰减。因此，我们着手研究由持续的经验依赖输入介导的突触维持机制。成熟小鼠须剥夺引起新皮层突触强度的衰减。我们发现，代谢性谷氨酸受体的关闭和神经元中肌醇三磷酸（IP3）信号的关闭参与了这种剥夺诱导的衰减。因此，由持续的晶须输入诱导的IP3信号对于维持突触功能是不可或缺的。

Synaptic functions should be maintained for the stable information processing in the brain. It is recognized that the shut down of experience inputs result in the attenuation of corresponding brain functions. We thus set out to investigate mechanisms underlying the synaptic maintenance mediated by ongoing experience-dependent inputs.Whisker deprivation in mature mice induced the attenuation of synaptic strength in the neocortex. We revealed that the shut down of metabotropic glutamate receptor and following inositol trisphosphate (IP3) signaling in neurons is involved in this deprivation-induced attenuation. Therefore, IP3 signaling induced by ongoing whisker inputs is indispensable for the maintenance of synaptic functions.