论文部分内容阅读
应用制霉菌素穿孔膜片钳全细胞记录技术研究了5－HT对急性分离的大鼠脊髓背角浅层（Ⅰ、Ⅱ层）神经元甘氨酸激活的全细胞电流的调控作用。实验结果表明：（1）在脊髓背角浅层神经元，甘氨酸作用于士的宁敏感型的甘氨酸受体，在钳制电位为-40mV时，可引起内向电流（IGly）；（2）5－HT呈浓度依赖性的增强Gly反应；（3）5－HT的增强作用既不改变IGly的平衡电位，也不影响Gly与受体的亲和力；（4）5－HT2受体激动剂α-甲基-5－HT能模拟5－HT的增强效应；而5－HT2受体的拮抗剂ketanserine可阻断5－HT对IGly的增强作用；（5）蛋白激酶C（PKC）的抑制剂chelerythrine可抑制5－HT对IGly的增强作用。本研究的结果说明：5－HT可呈浓度依赖性地增强大鼠脊髓背角浅层神经元的IGly，5－HT经5－HT2受体介导其对IGly的调控，脊髓背角浅层神经元内经PKC的信号转导途径在5－HT对IGly的增强效应中起重要的作用。本研究的结果提示5－HT和Gly的相互作用在脊髓水平的伤害性信息传递和调控过程中可能具有重要的意义。
The effect of 5-HT on the regulation of glycine-activated whole-cell currents in the neurons of acutely separated spinal cord dorsal horn (layers I, II) was studied using nystatin-perforated patch-clamp whole cell recording technique. The experimental results showed that: (1) glycine acted on strychnine-sensitive glycine receptors in the superficial neurons of spinal dorsal horn and induced inward current (IGly) at clamp potential of -40mV; (2) 5- HT enhanced the Gly response in a concentration-dependent manner; (3) the potentiation of 5-HT neither changed the equilibrium potential of IGly nor the affinity of Gly with the receptor; (4) the concentration of 5-HT2 receptor agonist α- (5) Inhibitors of protein kinase C (PKC), chelerythrine, can inhibit the enhancement of 5-HT. However, ketanserine, an antagonist of 5-HT2 receptor, can block the enhancement of 5-HT on IGly. Inhibit 5-HT on the enhancement of IGly. The results of this study indicate that 5-HT can enhance the expression of IGly in a dose-dependent manner in the superficial layers of the spinal dorsal horn of the rat spinal cord by 5-HT2 receptor. PKC signaling in neurons plays an important role in the potentiation of IGly by 5-HT. The results of this study suggest that the interaction of 5-HT and Gly may have important implications in the process of nociceptive transmission and regulation of spinal cord levels.