摘要
目的在50只成年Wister大鼠上,观察了侧脑室(icv)注射GABA(γ氨基丁酸)后,伏隔核(NAc)痛反应神经元放电的变化和荷包牡丹碱(Bic)对GABA作用的阻断效应,从而进一步研究GABA与NAc在痛觉调制中的作用。方法采用icv注射,电脉冲强直刺激坐骨神经作为伤害性痛刺激,玻璃微电极细胞外记录痛反应神经元放电的变化。结果(1)icv注入GABA能够使正常大鼠NAc中痛兴奋神经元(PEN)痛诱发放电频率减少、潜伏期延长,而使痛抑制神经元(PIN)痛诱发放电频率增加、诱发放电完全抑制时程缩短;(2)icv注入GABAA受体拮抗剂Bic能够阻断GABA的上述效应。结论(1)外源性GABA可使正常大鼠NAc中痛反应神经元对伤害性刺激的反应减弱,表现为镇痛效应;(2)GABA的这种镇痛作用主要是通过GABAA受体介导的。该结果揭示,GABA和NAc在痛觉调制中具有非常重要的作用。
Objective In order to further study the role of GABA(γ-aminobutyric acid) and the nucleus accumbens (NAc) in the painful modulation, the effects of GABA on electrical activities of the pain-related neurons in the NAc were studied in 50 Wistar rats. Methods Glassmicrodectrode extracellular recordings and intracerebroventricular (icv) injection methods were used in the experiment. Results (1) Icv injection of GABA caused the decrease in the pain-evoked discharge frequency and the prolongation of latency of pain-excitation neurons (PEN), while it increased the pain-evoked discharge frequency and shorten the inhibitory duration of pain-inhibition neurons (PIN) in the NAc of the normal rats. (2) Icv injection of GABA A-receptor antagonist (Bic) could antagonist the effects of GABA-induced. Conclusion (1) The exogenous GABA could weaken the responses of PEN in the NAc of rats to the noxious stimulation, expressing as analgesic effects. (2) The effects of GABA-induced were mediated by GABA A receptor. All these results revealed that GABA and the NAc played a very important role in the modulation of the algesia.
出处
《神经科学通报》
SCIE
CAS
CSCD
2005年第1期53-57,共5页
Neuroscience Bulletin
基金
国家自然科学基金资助
项目批准号:30240058
关键词
伏隔核
痛反应神经元
GABA
荷包牡丹碱
痛觉调制
nucleus accumbens (NAc)
pain-related neurons
GABA (γ-aminobutyric acid)
Bicuculline (Bic)