摘要
目的:研究大鼠脊髓对福尔马林痛刺激的反应及氯胺酮的影响。方法:采用福尔马林致痛模型、c-fos基因免疫组化法和NADPH-d组化技术。SD大鼠30只,分为福尔马林致痛组、痛刺激前和后腹腔注射氯胺酮组及相应对照组,取脊髓切片。结果:(1)痛刺激后,刺激侧脊髓背角出现大量Fos免疫样阳性(FLI)神经元,其中部分为FLI/NOS双标记神经元;(2)痛刺激之前或之后给予氯胺酮,背角各层FLI神经元和FLI/NOS双标记神经元的数量均显著减少。结论:同侧相应脊髓节段的某些神经元参与了化学性致痛信息的传导和调控,氯胺酮通过抑制这些神经元的活动而产生抗伤害作用。此作用与抑制脊髓内NOS阳性神经元的活性有关。
Objective: To study the effect of formalin stimulation on neurons of rat spinal cord and the regulation of ke-tamine. Methods: Formalin pain model was employed. Thirty Sprague-Dawley rats were randomly divided into 6 groups. Spinal cord slices were studied by c-fos oncogene immunohistochemical technique (ABC method) and NADPH-d histo-chemistry technique. Results: (l)After injection of formalin, a lot of Fos-like immunoreactive (FLI) neurons were found in the ipsilateral dorsal horn, some of them were FLI/NOS double-labelled neurons. Most of the FLI or FLI/NOS double-labelled neurons were observed in the medial part of Lamina Ⅰ and the outer lamina Ⅱ . (2)Either before or after injection of formain, ketamine significantly decreased the number of FLI and FLI/NOS double-labelled neurons in all laminas(P< 0.01). Conclusion: (1) Some neurons of the ipsilateral spinal dorsal horn participate in the transmission and mediation of pain signal, while ketamine can suppress the activities of these neurons and produce antinociceptive effect. (2) The antinociceptive function of ketamine may be caused by the activity depression of the NOS neurons in spinal cord.
出处
《解剖学杂志》
CAS
CSCD
北大核心
2003年第3期209-214,共6页
Chinese Journal of Anatomy
基金
国家自然科学基金(39970715)
江苏省科委自然基金(97088)