Cabot J B, Goff D M, Cohen D H
J Neurosci. 1981 Jul;1(7):760-70. doi: 10.1523/JNEUROSCI.01-07-00760.1981.
Recent evidence suggests that neurons within the ventromedial medulla give rise to an inhibitory pathway(s) which projects directly upon the sympathetic preganglionic neuropil. The present investigations were initiated to determine the effects of interrupting this pathway on the expression of a learned autonomic response, defensively conditioned cardioacceleration in the pigeon. Experiment I included two groups. Each experimental animal was trained concomitantly with a sham-operated control, and all birds received 100 trials of conditioning. Each conditioning trial consisted of a 6-sec light presentation followed immediately by a 0.5-sec foot shock. The first experimental group included birds with lesions involving the rostral medullary raphe nuclei (RMR), while the second included birds sustaining lesions of the caudal pontine raphe region (CPR). The principal findings were that (a) RMR-lesioned birds exhibited heart rate increases significantly greater than CPR-lesioned and control birds, (b) heart rate changes in CPR-lesioned birds were not significantly different from control values, and (c) RMR and CPR lesions did not affect base line heart rates significantly. Experiment II was undertaken to determine whether the elevated responsivity following RMR lesions represented a performance increment or an actual enhancement of associative learning. RMR-lesioned animals and their paired controls received 60 trials of sensitization training (explicitly unpaired lights and foot shocks) followed by 60 trials of conditioning. The primary result was that, independent of the training paradigm, RMR-lesioned animals, had significantly greater heart rate increases than control animals. In summary, the "lability" of heart rate changes following RMR lesions apparently is a performance effect and does not represent an enhancement of associative learning. Additionally, the data are consistent with the hypothesis that lesions of this midline medullary region disrupt a descending pathway important for the phasic reflex modulation of chronotropic cardiac responses to exteroceptive stimuli.
最近的证据表明，延髓腹内侧的神经元产生了一条抑制性通路，该通路直接投射到交感神经节前神经纤维网。开展本研究是为了确定中断该通路对习得性自主反应（鸽子防御性条件性心动过速）表达的影响。实验I包括两组。每只实验动物都与假手术对照组同时进行训练，所有鸟类都接受100次条件训练。每次条件训练包括6秒的光照呈现，随后立即给予0.5秒的足部电击。第一个实验组包括损伤延髓头端中缝核（RMR）的鸟类，而第二个实验组包括损伤脑桥尾端中缝区域（CPR）的鸟类。主要发现是：（a）RMR损伤的鸟类心率增加显著大于CPR损伤的鸟类和对照组鸟类；（b）CPR损伤的鸟类心率变化与对照值无显著差异；（c）RMR和CPR损伤对基线心率无显著影响。实验II旨在确定RMR损伤后反应性升高是代表表现增强还是关联学习的实际增强。RMR损伤的动物及其配对对照组接受60次敏感化训练（明确不配对的光照和足部电击），然后进行60次条件训练。主要结果是，无论训练范式如何，RMR损伤的动物心率增加都显著大于对照动物。总之，RMR损伤后心率变化的“易变性”显然是一种表现效应，并不代表关联学习的增强。此外，这些数据与以下假设一致，即该中线延髓区域的损伤破坏了一条对心脏变时性反应对外感受性刺激的相位反射调节很重要的下行通路。
