脊髓5-羟色胺受体参与延髓外侧网状核对大鼠心脏伤害性感受的下行性抑制调控

摘要

目的 观察脊髓水平5-羟色胺受体参与谷氨酸微注射激活延髓外侧网状核对大鼠心脏伤害性感受的下行性调控作用.方法 雄性SD大鼠随机分为5组:缓激肽组、缓激肽+谷氨酸组、缓激肽+麦角新碱组、缓激肽+谷氨酸+麦角新碱组、缓激肽+谷氨酸+溶媒组.谷氨酸微注射于延髓外侧网状核,联合鞘内注射,观察心包内缓激肽诱发大鼠心脏-躯体运动反射的变化,该反射以背斜方肌肌电(EMG)为观测指标;同时观察脊髓背角c-Fos的表达.结果 (1)与缓激肽组相比,鞘内注射5-羟色胺受体拮抗剂麦角新碱对EMG活动无影响,然而,谷氨酸微注射激活延髓外侧网状核剂量依赖性地抑制了心包内缓激肽诱发的EMG活动;同时,脊髓背角c-Fos表达显著减少(P＜0.05);(2)与缓激肽+谷氨酸组相比,鞘内注射麦角新碱后,部分反转了化学激活延髓外侧网状核对EMG活动的抑制作用;同时,脊髓背角c-Fos表达增加(P＜0.05).然而,鞘内注射溶媒后,心包内缓激肽诱发的EMG活动与脊髓背角c-Fos的表达无统计学意义(P＞0.05).结论 脊髓水平的5-羟色胺受体参与了延髓外侧网状核对大鼠心脏伤害性感受的下行性抑制调控作用.%Objective To investigate the role of the lateral reticular nucleus (LRN) in descending inhibition of cardiac nociception in rats and the involvement of spinal serotonergic receptors in the descending inhibition.Methods Male SD rats were randomly divided into 5 groups,namely bradykinin (BK) group,BK + glutamate group,BK + methysergide group,BK + glutamate + methysergide group,and BK + glutamate + vehicle group.The rats received glutamate microinjection in the LRN combined with the intrathecal injection of serotonergic receptor antagonist methysergide,and the changes in the cardiacsomatic motor reflex induced by intrapericardial BK injection were monitored by observing electromyogram (EMG) responses of the dorsal spinotrapezius muscle;c-Fos expression in the spinal dorsal horn was also tested.Results Compared with BK group,intra-LRN glutamate administration produced a significant inhibitory effect on intrapericardial BK-induced EMG in a dose-dependent manner,and c-Fos expression was significantly decreased in the spinal dorsal horn (P＜0.05).Compared with BK + glutamate group,intrathecal administration of methysergide significantly attenuated the inhibitory effect of chemical stimulation of the LRN on intrapericardial BK-induced EMG and increased c-Fos expression in the spinal dorsal horn (P＜0.05).Intrathecal administration of the vehicle did not produce any effect on EMG or c-Fos expression (P＞0.05).Conclusion The serotonergic receptors in the spinal cord are involved in LRN-mediated descending inhibition of cardiac nociception in rats.