抑制海马体或体内膜输入到核,可以逆转压力引起的多巴胺系统功能的变化
Hannah B Elam1,2,3, Alexandra M McCoy1, Angela M Boley1
1Department of Pharmacology, Center for Biomedical Neuroscience, University of Texas Health Science Center, San Antonio, TX, United States.
The international journal of neuropsychopharmacology
|May 23, 2025
概括
压力增加了体 (PVT) 的副腹腔核和体核 (NAc) 之间的连接,导致精神病症状. 抑制从腹部海马体 (vHipp) 或PVT向NAc的投射可以逆转这些由压力引起的变化.
科学领域:
- 神经科学是一个神经科学.
- 精神病学是一个精神病学.
- 多巴胺系统研究研究
背景情况:
- 精神病症状在创伤后应激障碍 (PTSD) 中很常见.
- 异常的中膜多巴胺系统调节是这些症状的基础.
- 室内海马体 (vHipp) 和 thalamus (PVT) 的准室内核调节多巴胺神经元活动.
研究的目的:
- 调查vHipp和PVT在压力诱导的多巴胺系统改变中的作用.
- 测试抑制vHipp-NAc或PVT-NAc投影是否可以逆转这些变化.
主要方法:
- 与压力相关的病理生理学被诱导在老鼠使用不可避免的脚震.
- 在vHipp和PVT中,神经元活动和电路协调被检查为后应激.
- 用NAc afferents的化学遗传抑制来评估功能逆转.
主要成果:
- 足部冲击应激增加了PVT和NAc之间的连贯性,长达48小时.
- 压力增加了VTA多巴胺神经元群活动.
- 化学遗传抑制vHipp-NAc或PVT-NAc投影逆转了压力诱导的多巴胺活性.
结论:
- 压力后增加的PVT-NAc连贯性可能会导致类似精神病的症状.
- 针对PVT或vHipp提供了与PTSD相关的精神病的潜在治疗策略.
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