轴突-轴突突突触输入通过结构和功能调整轴突初始段来驱动恒常性可塑性
bioRxiv : the preprint server for biology
|April 25, 2024
概括
大脑中的恒常性可塑性依赖于轴突初始段 (AIS). 来自吊灯细胞的特定GABAergic输入,但不是篮细胞,调整皮质神经元中的AIS,影响神经元刺激性和社会行为.
科学领域:
- 神经科学是一个神经科学.
- 细胞神经科学 细胞神经科学
- 突触性可塑性 突触性可塑性
背景情况:
- 功能性大脑网络的稳定性由恒温可塑性维持,在扰乱后恢复平衡.
- 投射神经元 (PyN) 的轴突初始段 (AIS) 动态调整以控制神经元发射特性.
- 直接突触输入到AIS在恒温性可塑性中的作用尚不清楚.
研究的目的:
- 调查皮层PyNs的AIS的直接突触输入是否可以诱导恒温性可塑性.
- 为了确定特定类型的GABAergic输入是否对AIS可塑性产生差异影响.
主要方法:
- 研究了从吊灯细胞 (ChCs) 和帕瓦尔胺阳性篮细胞中改变的GABAergic突触输入对皮质PyNs的影响.
- 评估了AIS形态的变化,电压关闭的通道表达和神经元刺激性.
- 相关的AIS调节时间与社会行为恢复,以响应ChC突触传输变化.
主要成果:
- 来自ChCs的GABAergic输入的变化,但不是篮细胞,足以在1-2周内诱导AIS的恒常调整.
- AIS调整表现为形态变化,通道表达和PyN刺激性的改变.
- 在前额叶皮层PyNs中AIS调整的时间恰逢由修改的ChC突触传输引起的社会行为缺陷的恢复.
结论:
- 在 postsynaptic PyNs 中,AIS 的恒常性可塑性可以由特定的GABAergic输入驱动,特别是来自ChCs.
- 这种AIS调机制可能会抵消由不平衡的CHC前突触输入引起的神经元功能障碍.
- 作为对网络状态变化的反应,AIS可塑性代表了一个关键的恒温机制.
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