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通过刺激从中杏仁核/迈内特基底核到脑桥网状结构的兴奋性通路来增强听觉惊吓反应。

Enhancement of the acoustic startle response by stimulation of an excitatory pathway from the central amygdala/basal nucleus of Meynert to the pontine reticular formation.

作者信息

Koch M, Ebert U

机构信息

Tierphysiologie, Universität Tübingen, Germany.

出版信息

Exp Brain Res. 1993;93(2):231-41. doi: 10.1007/BF00228390.

Abstract

The acoustic startle response (ASR) is a simple motor reaction to intense and sudden acoustic stimuli. The neural pathway underlying the ASR in rats is already fairly well understood. As the ASR is subject to a variety of modulations, this reaction can serve as a model for vertebrate neuroethologists to investigate the neural mechanisms mediating sensorimotor transfer and their extrinsic modulation. We report here on experiments in rats which were undertaken in order to investigate the neural mechanisms underlying the enhancement of the ASR. An increased amplitude of the ASR can be observed during states of conditioned and unconditioned fear. By employing neuroanatomical tract-tracing methods, we describe a pathway from neurons of the medial division of the central amygdaloid nucleus (cA) and the basal nucleus of Meynert (B) to the caudal pontine reticular nucleus (PnC), an important relay station in the acoustic startle pathway. Extracellular recordings from acoustically responsive neurons in the PnC showed that electrical stimulation of the cA/B facilitates the tone-evoked response of these neurons. Behavioural tests following chemical stimulation of the cA/B with NMDA (N-methyl-d-aspartate) in awake rats indicated that activation of this pathway increases the ASR. The lack of sufficient spatial resolution of our stimulation techniques did not allow us to differentiate the relative contributions of the cA and the B to this effect. As the amygdaloid complex has been implicated in emotional behaviour, particularly in the mediation of fear, these findings substantiate the concept that the amygdaloid complex plays a key role for the enhancement of the ASR by conditioned and unconditioned fear.

摘要

听觉惊吓反应(ASR)是对强烈且突然的听觉刺激的一种简单运动反应。大鼠ASR背后的神经通路已得到相当充分的了解。由于ASR会受到多种调制,这种反应可作为脊椎动物神经行为学家研究介导感觉运动转换及其外在调制的神经机制的模型。我们在此报告对大鼠进行的实验,以研究ASR增强背后的神经机制。在条件性和非条件性恐惧状态下可观察到ASR幅度增加。通过采用神经解剖学示踪方法,我们描述了一条从中杏仁核内侧部(cA)和迈内特基底核(B)的神经元到脑桥尾侧网状核(PnC)的通路,PnC是听觉惊吓通路中的一个重要中继站。对PnC中听觉反应神经元的细胞外记录表明,电刺激cA/B可促进这些神经元的音调诱发反应。在清醒大鼠中用N-甲基-D-天冬氨酸(NMDA)对cA/B进行化学刺激后的行为测试表明,该通路的激活会增加ASR。我们刺激技术的空间分辨率不足,无法区分cA和B对这种效应的相对贡献。由于杏仁核复合体与情绪行为有关,特别是在恐惧的介导中,这些发现证实了杏仁核复合体在条件性和非条件性恐惧增强ASR中起关键作用的概念。

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