神经 Tac2 控制由慢性社会隔离压力引起的分布式大脑状态
Moriel Zelikowsky1, May Hui1, Tomomi Karigo1
1Division of Biology and Biological Engineering 156-29, California Institute of Technology, Pasadena, CA 91125, USA.
Cell
|May 19, 2018
概括
慢性社会隔离压力 (SIS) 通过在整个大脑上调高基尼2 (Tac2) /神经基尼B (NkB) 来改变小鼠的行为. 阻断NkB受体 (Nk3R) 逆转了这些效应,表明了治疗潜力.
科学领域:
- 神经科学
- 行为科学
- 分子生物学
背景情况:
- 长期的社会隔离会给人类带来严重的心理困扰,但其潜在的神经机制尚未完全理解.
- 了解社会隔离的神经生物学对于开发有效干预至关重要.
研究的目的:
- 在老鼠中研究由慢性社会隔离压力 (SIS) 引起的行为变化的神经基础.
- 探索塔基宁2 (Tac2) /神经基因B (NkB) 系统在SIS中介作用的作用.
主要方法:
- 在老鼠中诱导社会隔离压力 (SIS) 持续时间不同 (24小时与2周).
- 一种神经素3受体 (Nk3R) 抗剂的全身使用.
- 在小鼠群体中增强NKB表达和释放.
- 对多个大脑区域的Tac2/NkB功能进行多重分析.
主要成果:
- 两周的SIS, 而不是24小时, 导致显著的行为变化和大脑范围的Tac2/NkB升高.
- 使用NK3R抗剂可以预防大多数SIS诱导的行为变化.
- 增加的NkB信号模仿SIS效应, 促进侵略性和改变防御性行为.
- Tac2/NkB和Nk3R在调解不同SIS诱导的行为变化方面表现出特定区域的作用.
结论:
- Tac2/NkB信号传递是慢性社会隔离压力的行为和神经适应的一个关键媒介.
- Tac2/NkB系统以分布式的方式在多个大脑区域工作,以协调对SIS的反应.
- 对于与社会隔离相关的疾病,NK3R抗剂是一个有前途的治疗策略.
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