Kungel M, Ebert U, Herbert H, Ostwald J
Department of Animal Physiology, University of Tübingen, FRG.
Brain Res. 1994 Apr 18;643(1-2):29-39. doi: 10.1016/0006-8993(94)90005-1.
In this study we investigated the effects of possible modulatory transmitters on acoustically responsive neurons of the caudal pontine reticular nucleus (PnC). From previous work in our laboratory it has been suggested that the acoustically responsive giant neurons of this nucleus are the sensorimotor interface mediating the acoustic startle response. Furthermore they are the site of some of the modulatory influence impinging on this response. Besides a possibly glutamatergic excitation from the amygdala a cholinergic input from the midbrain has been described which may use substance P as cotransmitter. Therefore we used electrophysiological and histochemical methods to study this possible modulatory influence in the caudal pontine reticular nucleus. In the first part of this study we recorded extracellularly from single units in the PnC in vivo and studied the effects of iontophoretically applied transmitters. Substance P elicited a long lasting excitation. This excitatory effect of SP was potentiated by acetyl-beta-methylcholine (AMCh, an acetylcholine agonist), whereas single application of AMCh showed no uniform response. Glutamate elicited a potent brief excitation, while application of GABA showed a potent brief inhibition of PnC neurons. In the second part of this study we employed immunoperoxidase staining for substance P, which revealed a fairly dense network of substance P-immunoreactive (SP-ir) fibers in the lateral and ventral aspects of the PnC. Combining retrograde tracing and immunocytochemistry for substance P, we demonstrated that the SP-ir axons in the PnC originate mainly in the laterodorsal tegmental nucleus. We therefore conclude that activation of the laterodorsal tegmental nucleus may facilitate the acoustic startle response by a long lasting excitation of neurons in the caudal pontine reticular nucleus.
在本研究中，我们调查了可能的调制性递质对尾侧脑桥网状核（PnC）听觉反应神经元的影响。根据我们实验室之前的研究工作，有人提出该核团中对声音有反应的巨型神经元是介导听觉惊吓反应的感觉运动接口。此外，它们也是对该反应产生一些调制性影响的部位。除了来自杏仁核可能的谷氨酸能兴奋外，还描述了来自中脑的胆碱能输入，其可能以P物质作为共递质。因此，我们使用电生理和组织化学方法来研究尾侧脑桥网状核中这种可能的调制性影响。在本研究的第一部分，我们在体内对PnC中的单个神经元进行细胞外记录，并研究离子电泳施加递质的影响。P物质引发了持久的兴奋。SP的这种兴奋作用被乙酰-β-甲基胆碱（AMCh，一种乙酰胆碱激动剂）增强，而单独应用AMCh则没有一致的反应。谷氨酸引发了强烈的短暂兴奋，而应用GABA则对PnC神经元表现出强烈的短暂抑制。在本研究的第二部分，我们采用P物质免疫过氧化物酶染色，结果显示在PnC的外侧和腹侧有相当密集的P物质免疫反应性（SP-ir）纤维网络。结合逆行追踪和P物质免疫细胞化学，我们证明PnC中的SP-ir轴突主要起源于外侧背侧被盖核。因此，我们得出结论，外侧背侧被盖核的激活可能通过对尾侧脑桥网状核神经元的持久兴奋来促进听觉惊吓反应。
