经过急性压力后的普遍恐惧是由神经元共传递体身份的变化引起的
Hui-Quan Li1,2, Wuji Jiang1,2, Li Ling1,2
1Neurobiology Department, School of Biological Sciences and Center for Neural Circuits and Behavior, University of California San Diego, La Jolla, CA 92093, USA.
概括
焦虑症的普遍恐惧源于大脑干神经元中的传感器开关. 在患有PTSD的小鼠和人类中观察到这种涉及谷氨酸和GABA的切换, 提供了新的治疗点.
科学领域:
- 神经科学
- 分子精神病学
- 焦虑 疾病
背景情况:
- 焦虑症的特征是将恐惧概括为无害的刺激.
- 恐惧泛化的基本神经生物学机制仍然很大程度上未知.
研究的目的:
- 阐明导致恐惧普遍化的细胞和分子机制.
- 确定潜在的焦虑症治疗点,
主要方法:
- 在急性应激的小鼠模型中,研究了背部拉菲核的血清神经元的发射器身份变化.
- 从被诊断患有创伤后应激障碍 (PTSD) 的人身上检查死亡后的大脑组织.
- 评估操纵已识别的发射器开关对恐惧概括行为的影响.
主要成果:
- 在小鼠中,一般性恐惧是通过从谷氨酸转换为胺黄油酸 (GABA) 的脊髓神经元.
- 在人类PTSD大脑样本中发现了类似的发射开关.
- 阻断这种发射开关可以防止恐惧的发展.
- 皮质激素和葡萄皮质激素受体的激活与这种转换有关.
- 抗抑郁药物治疗有效地阻断了传感器的转换和随后的恐惧泛化.
结论:
- 恐惧的泛化涉及到关键脑干电路中的特定神经化学转变.
- 在焦虑和PTSD的病理生理学中,
- 针对这种转换提供了一个有前途的治疗策略来治疗焦虑症.
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