周围注射氯氨酮对皮下注射蜜蜂毒引起的猫脊髓广动力阈神经元长时程持续性放电增强的抑制效应(英文)

通过应用单细胞细胞外电生理记录 ,在乌拉坦 -氯醛糖合剂麻醉状态下 ,对在猫后爪局部注射单一剂量的氯氨酮对皮下注射蜜蜂毒引起的背角 WDR神经元放电增强的抑制作用进行了研究。在 WDR神经元周围感受野皮下注射蜜蜂毒可诱发出超过背景放电 1小时的单相持续性放电增强。在感受野中心蜜蜂毒注射部位用氯氨酮 ( 10 0 mmol/L,0 .1ml)局部预处理组 ( 3 .10± 0 .42放电数 /秒 ,n=5 )与盐水对照组 ( 7.61± 0 .17放电数 /秒 ,n=5 )相比对神经元的放电增强可大幅度地抑制 60 %。而且 ,用相同剂量的氯氨酮局部后处理组 ( 1.5 1± 0 .0 6放电数 /秒 ,n=5 )与盐水对照组 ( 7.76± 0 .15放电数 /秒 ,n=5 )相比 ,对神经元的放电增强可明显抑制 81%。不过 ,用相同剂量的氯氨酮在未经蜜蜂毒处理的对侧后爪相应区域皮下给药 ,对 WDR神经元放电增强不产生任何影响 ,提示局部注射氯氨酮的抑制效应并非是全身效应的结果。目前的结果提示 ,氯氨酮除了部分地通过阻断钠离子和电压敏感性钙通道的作用外 ,主要通过周围 NMDA受体发挥它的局部镇痛效应。

PERIPHERALLY SUPPRESSIVE EFFECTS OF KETAMINE ON SUBCUTANEOUS BEE VENOM-INDUCED PROLONGED,PERSISTENT FIRING OF SPINAL WIDE-DYNAMICRANGE NEURONS IN THE CAT

By using extracellular single unit recording technique, locally suppressive effects of a single dose of ketamine on sub-cutaneous (s. c. ) bee venom-induced increase in firing of wide dynamic-range (WDR) neurons in spinal dorsal horn were investi-gated on urcthane-chloralose anesthetized cats. Injection of bee venom s.c. into the cutaneous receptive field (RF) resulted in asingle phase of prolonged, persistently increased firing of WDR neurons over background activity for more than 1 h. Local pre-treatment with ketamine (100 mM, 0. 1 m l) into the center of RF where bee venom was injected produced a dramatic suppressionof the increased neuronal firing by 60% (3.10± 0.42 spikes/s, n= 5) when compared with saline pre-treated group (7.61 ± 0.17spikes/ s. n = 5 ). Moreover, local post-treatment with the same dose of ketamine also produced a profound suppression of the in-creased neuronal activity by 81% (1.51±0.06 spikes/s, n=5) when compared with the saline post-treated group (7.76±0.15spikes s, n=5). However, s.c. administration with the same dose of ketamine into a symmetrical region on the bee venom un-treated contralateral hindpaw produced no affection on the increased firing of the WDR neurons, suggesting that the suppressiveaction of local ketamine was not the result of systemic effects. The present result suggests that ketamine may exert its localantinociceptive effects mainly through the peripheral NMDA receptors in addition to its partially potential blocking effects onsodium and voltage-sensitive calcium channels.