根据蓝斑刺激可以通过脊髓下行性去甲肾上腺素能纤维阻断由背角上传到束旁核神经元的伤害性放电的事实 ,本实验用脊髓鞘内给予相应工具药的方法 ,进一步分析了上述下行性抑制作用在脊髓背角中阻止伤害性传入信号向上传递的可能机制 ,结果发现 :(1)鞘内注入ATP 敏感钾通道阻断剂格列苯脲或腺苷受体拮抗剂氨茶碱 ,均可以阻断或取消刺激蓝斑引起的对束旁核伤害性放电的抑制作用 ;(2 )鞘内注入ATP 钾通道激动剂nicorandil或腺苷受体激动剂 5′ N ethylcarboxamido adenosine (NECA) ,都可抑制束旁核神经元的伤害性放电 ;(3)鞘内注入氨茶碱可阻断鞘内注入nicorandil引起的束旁核痛放电的抑制 ,而鞘内注入格列苯脲不能阻断鞘内注入NECA引致的束旁核痛放电的抑制。这些结果提示 :(1)蓝斑刺激在脊髓背角中抑制痛信号的上传 ,要有ATP 敏感钾通道的激活和内源性腺苷的释放为中介 ;(2 )ATP 敏感钾通道的激活发生在腺苷的释放之前 Based on the fact that locus coeruleus stimulates descending noradrenergic fibers in the spinal cord to block the nociceptive discharge from the dorsal horn to neurons in the parafascicular nucleus, we further analyzed the The above-mentioned descending inhibitory effect in spinal dorsal horn to prevent the transmission of nociceptive signals up the possible mechanism and found that: (1) intrathecal injection of ATP-sensitive potassium channel blocker glibenclamide or adenosine receptor antagonist ammonia Theophylline can block or cancel the inhibitory effect on the parabronchial nucleus caused by locus coeruleus stimulated by locus coeruleus injection; (2) Intrathecal injection of nicorandil or adenosine receptor agonist 5 ’N ethylcarboxamido adenosine NECA) could inhibit the nociceptive discharge of neurons in parafascicular nucleus. (3) Intrathecal injection of aminophylline blocked the inhibition of parathyroidectoral discharge induced by intrathecal nicorandil, whereas intrathecal injection of glibenclamide Can not block intrathecal injection of NECA induced parathyroid nuclear pain inhibition of discharge. These results suggest that (1) locus coeruleus suppresses the uptake of pain signals in the dorsal horn of the spinal cord, with the activation of ATP-sensitive potassium channels and the release of endogenous adenosine as mediators; (2) activation of ATP-sensitive potassium channels occurs at Before adenosine release