Vagal afferent modulation of spinal nociceptive transmission in the rat.
Vagal afferent modulation of spinal nociceptive transmission in the rat.
复制标题
大鼠脊髓伤害性传递的迷走神经传入调节。
DOI：
10.1152/jn.1989.62.2.401
复制
发表时间：
1989
影响因子：
2.5
通讯作者：
Gebhart,GF
中科院分区：
文献类型：
--
作者：
Ren,K;Randich,A;Gebhart,GF
1.在戊巴比妥钠和乌拉坦麻醉的瘫痪大鼠上，观察了迷走神经传入刺激对脊髓伤害性信息传递的影响和脊髓通路(S)介导的伤害性传入效应。被研究的60个单位对机械刺激和皮肤感受野的有害加热(50摄氏度)做出反应，这些感受野仅限于脚趾和脚垫的无毛皮肤。记录部位位于L3-L5脊髓节段的I-VI板层。2.VAS促进和抑制神经元对热的反应。在戊巴比妥钠麻醉的大鼠，大多数(24/44)单位的反应被低强度的VAS促进，而被高强度的VAS抑制。部分单位(15/44)仅被VAS抑制，而另一些单位(4/44)仅被VAS促进。VAS产生的抑制依赖于强度、脉冲宽度、频率和刺激持续时间。在乌拉坦麻醉大鼠，6/16个单位的反应最初被促进，然后随着VAS强度的增加而抑制，其中9个单位的反应被VAS抑制。两种麻醉条件下的招募指数、平均抑制阈值和抑制单位对热反应的平均强度的定量比较显示，两种麻醉条件之间没有显著差异。3.VAS对神经元热反应的影响与其对血压的影响是分离的。不管VAS对伤害性高温的单位反应有何影响，VAS始终产生强度依赖的降压反应。通过累加和技术和刺激前时间直方图逐个分析来确定VAS开始抑制和促进的潜伏期。抑制潜伏期为91+/-11(SE)ms，促进潜伏期为278+/-59 ms，均发生在血压变化之前。最后，将利多卡因微量注射到胸髓腹外侧索(VLF)或横断胸髓背外侧索(DLF)可减弱VAS对神经元的反应，但不影响VAS的降压反应。4.研究了11个背角单位对皮肤分级伤害性加热的反应，在所研究的温度范围内(42-52℃)，刺激-反应函数(SRF)是线性的和单调的。在抑制单位对热反应的强度下，VAS显着降低了SRF的斜率。在促进单位对热的反应的强度下，产生了SRF的左移，平行移动。
1. The effects of vagal afferent stimulation (VAS) on spinal nociceptive transmission and the spinal pathway(s) mediating VAS-produced effects were examined in pentobarbital sodium- and urethane-anesthetized, paralyzed rats. The 60 units studied responded to mechanical stimuli and noxious heating (50 degrees C) of cutaneous receptive fields confined to the glabrous skin of the toes and footpads. Recording sites were located in laminae I-VI of the L3-L5 spinal segments. 2. VAS facilitated and inhibited neuronal responses to heat. In pentobarbital-anesthetized rats, responses of most (24/44) units were facilitated by low and inhibited by higher intensities of VAS. Responses of some units (15/44) were only inhibited and others (4/44) only facilitated by VAS. Inhibition produced by VAS was intensity-, pulse width-, frequency-, and stimulation duration-dependent. In urethane-anesthetized rats, responses of 6/16 units were initially facilitated, then inhibited as the intensity of VAS was increased; responses of nine units were inhibited by VAS. Quantitative comparisons of recruitment indices, mean thresholds for inhibition and mean intensities to inhibit unit responses to heat to 50% of control revealed no significant differences between the two anesthetic conditions. 3. The effects of VAS on neuronal responses to heat were dissociable from its effect on blood pressure. Regardless of the effect of VAS on unit responses to noxious heat, VAS consistently produced intensity-dependent depressor responses. The latencies to onset of inhibition and facilitation by VAS were determined by a cumulative sum technique and bin-by-bin analysis of peristimulus time histograms. The apparent latencies were 91 +/- 11 (SE) ms for inhibition and 278 +/- 59 ms for facilitation, both of which occurred before changes in blood pressure. Finally, microinjections of lidocaine into the ventrolateral funiculus (VLF) or transections of the dorsolateral funiculus (DLF) of the thoracic spinal cord attenuated VAS-produced effects on neuronal responses, but did not affect VAS-induced depressor responses. 4. The responses of 11 dorsal horn units to graded noxious heating of the skin were studied; the stimulus-response functions (SRF) were linear and monotonic throughout the temperature range examined (42-52 degrees C). VAS at intensities which inhibited unit responses to heat significantly decreased the slope of the SRF. VAS at intensities which facilitated unit responses to heat produced a leftward, parallel shift of the SRF.(ABSTRACT TRUNCATED AT 400 WORDS)