Morgan Michael M, Fields Howard L
Departments of Neurology and Physiology and The W.M. Keck Center for Integrative Neuroscience, University of California, San Francisco, CA 94143-0114 USA.
Pain. 1993 Jan;52(1):1-9. doi: 10.1016/0304-3959(93)90108-2.
A wide range of environmental stimuli have been shown to induce antinociception. Investigation of the brain regions contributing to environmentally induced antinociception (EIA) has focused primarily on the effect of disrupting neural transmission at various CNS sites. In contrast, the present study analyzed changes in the activity of nociceptive modulatory neurons in the rostral ventromedial medulla (RVM) following induction of antinociception by a physiological stimulus, volume expansion. Previous research indicates that 2 classes of RVM neuron, the on- and off-cells, facilitate and inhibit nociception, respectively. In the present study, volume expansion induced by intravenous administration of Ficoll inhibited the tail-flick reflex in 17 of 21 rats and simultaneously increased the firing rate of off-cells and decreased that of on-cells. Changes in cell activity occurred only in those rats in which antinociception was produced. Lidocaine inactivation of the RVM did not block antinociception produced by Ficoll infusion. These findings demonstrate that, although antinociception produced by physiological activation of vagal afferents is associated with an increase in off-cell and a decrease in on-cell activity, these changes are not required for volume expansion-induced antinociception.
多种环境刺激已被证明可诱导抗伤害感受。对参与环境诱导性抗伤害感受（EIA）的脑区的研究主要集中在破坏中枢神经系统（CNS）各个部位神经传递的影响上。相比之下，本研究分析了生理刺激——容量扩张诱导抗伤害感受后，延髓头端腹内侧区（RVM）中伤害性调制神经元活动的变化。先前的研究表明，RVM中的两类神经元，即开细胞和关细胞，分别促进和抑制伤害感受。在本研究中，静脉注射右旋糖酐诱导的容量扩张抑制了21只大鼠中17只的甩尾反射，同时增加了关细胞的放电频率，降低了开细胞的放电频率。细胞活动的变化仅发生在产生抗伤害感受的那些大鼠中。RVM的利多卡因失活并未阻断右旋糖酐输注产生的抗伤害感受。这些发现表明，虽然迷走神经传入纤维的生理激活产生的抗伤害感受与关细胞活动增加和开细胞活动减少有关，但容量扩张诱导的抗伤害感受并不需要这些变化。
