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在牙状环颗粒细胞的突触可塑性到体静止素表达的内部神经元突触支持对象位置记忆

Gayane Grigoryan¹, Harumi Harada², H Sophie Knobloch-Bollmann¹

¹Laboratory of Systems & Cellular Neuroscience, Institute for Physiology I, Medical Faculty, University of Freiburg, Freiburg 79104, Germany.

Proceedings of the National Academy of Sciences of the United States of America

|December 13, 2023

概括

甲基酸盐受体1α (mGluR1α) 对于海马体的突触可塑性至关重要,增强记忆力. 这种受体介导长期增强纤维-体静止素内部神经突触的作用,支持对象位置记忆.

科学领域:

神经科学是一个神经科学.
突触性可塑性突触性可塑性
记忆研究记忆研究

背景情况:

牙状回形 (DG) 中的索马托斯塔丁表达性内神经元 (SOMI) 调节海马网络活动.
摩西纤维 (MF) 对SOMI的突触对于总局的信息处理至关重要.
在记忆中的MF-SOMI突触中,活动依赖可塑性的作用仍然在很大程度上是未知的.

研究的目的:

调查MF-SOMI突触中突触可塑性的基础分子机制.
为了确定甲基酸盐受体 (mGluRs) 在MF-SOMI突触可塑性中的作用.
阐明MF-SOMI可塑性对海马体记忆功能的贡献.

主要方法:

在小鼠海马片中的电生理学记录.
对mGluR1α和mGluR5.5的药理学操纵
对细胞内信号通路 (Ca2+,ERK1/2) 的评估.
在DG-SOMI中对mGluR1α进行基因操纵 (shRNA淘汰).
行为测试 (对象位置记忆).

主要成果:

mGluR1α,但不是mGluR5,对于诱导MF-SOMI突触的关联长期强化 (LTP) 是必不可少的.
在MF-SOMI突触中的LTP是以后突触介导的,需要Ca2+流入,G蛋白信号传递,Ca2+依赖的ERK1/2激活和NMDA受体活性.
在DG-SOMI中抑制mGluR1α取消了MF-SOMI LTP,减少了SOMI招募,并损害了对象位置记忆.

结论:

后突触mGluR1α信号传输是MF-SOMI突触中的可塑性的关键调解器.
依赖mGluR1α的MF-SOMI可塑性对于依赖牙状环的记忆形成至关重要,特别是对象位置记忆.

关键词:

有牙的吉鲁斯.内部神经元内部神经元 mGluR1α 的使用情况.对象的位置记忆物体的位置记忆突触性可塑性突触性可塑性

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