Birnbaum S G, Davis M
Interdept. Neuroscience Program, Yale University School of Medicine, Connecticut Mental Health Center, New Haven 06508, USA.
Brain Res. 1998 Jan 26;782(1-2):318-23. doi: 10.1016/s0006-8993(97)01309-7.
The amplitude of the acoustic startle reflex can be modulated by exposure to aversive stimuli or other conditions which evoke a state of fear. The neurotransmitters involved in this modulation are currently being investigated. Unilateral local infusion of corticotropin-releasing hormone (CRH; 0, 10, 20, 40 and 80 ng) into the nucleus reticularis pontis caudalis (PnC), an obligatory synapse in the acoustic startle reflex, significantly elevated startle amplitude in a dose-dependent manner. The facilitation of startle began immediately following infusion, reached asymptote approximately 20-25 min later, and persisted throughout the remaining 60 min test session. This CRH-enhanced startle effect was blocked by infusion of the CRH antagonist, alpha-helical CRH9-41, immediately prior to CRH infusion. These results support an involvement of CRH at the level of the PnC in modulating the acoustic startle reflex.
通过暴露于厌恶刺激或其他引发恐惧状态的条件下，可调节听觉惊吓反射的幅度。目前正在研究参与这种调节的神经递质。将促肾上腺皮质激素释放激素（CRH；0、10、20、40和80纳克）单侧局部注入脑桥尾侧网状核（PnC），这是听觉惊吓反射中的一个必需突触，可显著以剂量依赖方式提高惊吓幅度。惊吓促进作用在注入后立即开始，约20 - 25分钟后达到稳定状态，并在剩余的60分钟测试期间持续存在。在注入CRH之前立即注入CRH拮抗剂α - 螺旋CRH9 - 41可阻断这种CRH增强的惊吓效应。这些结果支持CRH在PnC水平参与调节听觉惊吓反射。
