大脑衍生神经营养因子尺度预突触过渡物调节激发性神经传递
Camille S Wang1,2, Clara I McCarthy1,2, Natalie J Guzikowski1,2
1Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN 3729-7933.
概括
大脑衍生神经营养因子 (BDNF) 通过增加通过TrkB信号的前突触流量来增强唤起的神经传递. 慢性BDNF-TrkB通路抑制可以选择性地减少引起的谷氨酸释放,影响突触功能.
科学领域:
- 神经科学是一个神经科学.
- 突触生理学 突触生理学
- 分子生物学分子生物学
背景情况:
- 大脑衍生神经营养因子 (BDNF) 对突触功能至关重要,并与神经精神疾病有关.
- 对于BDNF在前突触终端控制神经传递的特定作用,尚未完全阐明.
研究的目的:
- 为了研究BDNF在突触前终端的精确功能.
- 确定BDNF-TrkB信号传递对唤起和自发神经递质的影响.
- 为了确定BDNF前突触效应背后的机制.
主要方法:
- 在海马细胞培养中的单突触动态的光学成像.
- 外源BDNF的应用和内源BDNF-TrkB信号的急性/慢性阻断.
- 使用了有条件的TrkB淘汰赛小鼠线和电压通路 (VGCC) 的药理阻塞剂.
主要成果:
- 外源BDNF选择性增强唤起了,但不是自发的,刺激性神经传递.
- 慢性抑制BDNF-TrkB信号传递显著降低了引起的谷氨酸释放,同时节省了自发释放.
- 慢性BDNF-TrkB阻断选择性地减少引起的过渡体,由P/Q型VGCCs介导.
结论:
- BDNF-TrkB活性通过增加突触前VGCC活性来选择性地增强唤起的谷氨酸释放.
- 这项研究强调了慢性信号在BDNF的前突触功能中的重要性.
- 这些发现提供了关于BDNF在调节神经传递和潜在治疗点中的作用的见解.
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