Objective: To observe the effects of gamma-aminobutyric acid (GABA) on the electric activities of pain-excited neurons (PEN) in nucleus accumbens (NAc) in central nervous system (CNS) of morphine-dependent rats.
Methods: After GABA or the GABA(A)-receptor antagonist, bicuculline (Bic), was injected into cerebral ventricles or NAc, right sciatic nerve was stimulated by electrical pulses, which was considered as traumatic pain stimulation. Extracellular recordings methods were used to record the electric activities of PEN in NAc.
Results: When GABA was injected into intracerebroventricle (ICV) as well as NAc, it could decrease the pain-evoked discharge frequency and prolong the latency of PEN. Bic could interdict the above effects of GABA on the electric activities of PEN.
Conclusion: Exogenous GABA might have an inhibitory effect on the central pain adjustment. Furthermore, GABA and GABA(A) receptor participate and mediate the traumatic information transmission process in CNS.
目的: 观察γ-氨基丁酸(γ-aminobutyric acid, GABA)对吗啡依赖大鼠中枢神经系统伏隔核(nucleus accumbens, NAc)痛兴奋神经元(pain-excited neurons, PEN)电活动的影响。
方法: 脑室或NAc 中注射GABA 或荷包牡丹碱(bicuculline, Bic), 电脉冲刺激右侧坐骨神经作为伤害性疼痛刺激, 用玻璃微电极在细胞外记录中枢神经系统伏隔核痛兴奋神经元电活动的变化。
结果: 脑室及NAc 中注入GABA 均能使吗啡依赖大鼠NAc 中PEN 潜伏期延长、 痛诱发放电频率减少; GABAA受体拮抗剂Bic能够阻断GABA的上述效应。
结论: 外源性GABA在中枢痛觉调制中起抑制作用, GABA及GABAA受体参与介导中枢伤害性信息的传递过程。