IGF1介导了嗅觉社会学习记忆中僧帽细胞的突出可塑性过程
IGF1-Dependent Synaptic Plasticity of Mitral Cells in Olfactory Memory during Social Learning
背景
在社会交往传播的食物偏好(STFP)期间，小鼠对食物气味的长期记忆是通过社会交往同伴提供的。大脑如何将社会环境与气味信号联系起来，以促进记忆编码?
方 法
在SFTP期间，本文采用特定的气味暴露。在嗅球中，有选择性地将具有突触强度的肾小球特异性长时程增强（LTP）介导于颗粒和僧帽细胞的树突状突触体的GABA能神经元上。
结 果
突触结合蛋白-10、 僧帽细胞的IGF1分泌的钙离子传感器或嗅球IGF1受体的缺失不仅能抑制社会相关的GABA能神经元长时程增强，还能损害STFP后记忆的形成。相反，通过增强突触后GABA受体反应，将IGF1注入到急性嗅球切片中，就能在僧帽细胞中产生GABA能神经元LTP。
结 论
因此，我们的研究揭示了一个作用于感觉信息处理最初阶段的社会相关长时记忆的突触底物。
原始文献摘要
BACKGROUND: During social transmission of food preference (STFP),mice form long-term memory of food odors presented by a social partner. How does the brain associate a social context with odor signals to promote memory encoding?
METHODS: Here we show that odor exposure during STFP, but not unconditioned odor exposure, induces glomerulus-specific long-term potentiation (LTP) of synaptic strength selectively at the GABAergic component of dendrodendritic synapses of granule and mitral cells in the olfactory bulb.
RESULTS: Conditional deletion of synaptotagmin-10, the Ca2+ sensor for IGF1 secretion from mitral cells, or deletion of IGF1 receptor in the olfactory bulb prevented the socially relevant GABAergic LTP and impaired memory formation after STFP. Conversely, the addition of IGF1 to acute olfactory bulb slices elicited the GABAergic LTP in mitral cells by enhancing postsynaptic GABA receptor responses.
CONCLUSIONS: Thus, our data reveal a synaptic substrate for a socially conditioned long-term memory that operates at the level of the initial processing of sensory information.
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