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应用制霉菌素(nystatin)穿孔全细胞记录方法,研究了N-甲基-D-门冬氨酸(NMDA)对新鲜分离的大鼠骶髓后连合核(SDCN)神经元γ-氨基丁酸(GABA)激活的全细胞电流的调控.实验结果如下:(ⅰ) 在无Mg2+及含1 μmol/L甘氨酸的标准细胞外液中,当钳制电位为-40 mV时,NMDA(100 μmol/L)可抑制GABA和muscimol (Mus)在SDCN神经元激活的全细胞电流(IGABA和IMus),且NMDA受体的竞争性拮抗剂D-2-amino-5-phosphonovalerate(APV,100 μmol/L)可完全阻断NMDA激活的电流,并可消除NMDA对IGABA的抑制作用.(ⅱ)当细胞外液中无Ca2+及待测神经元被Ca2+螯合剂BAPTA AM预处理2 h后,NMDA对IGABA的抑制作用消失;而用电压依赖性钙通道阻断剂Cd2+(10 μmol/L)或La3+(30μmol/L)预处理后,NMDA对IGABA的抑制作用仍然存在.(ⅲ) NMDA对IGABA的抑制作用可被钙-钙调素依赖性蛋白激酶Ⅱ(CaMKⅡ)的抑制剂KN-62所阻断.提示在大鼠SDCN神经元,NMDA对IGABA的抑制作用为一Ca2+依赖性的过程,这一过程的"下游"机制与细胞内CaMKⅡ有关.揭示了Ca2+和CaMKⅡ分别作为细胞内第二信使和第三信使将NMDA受体和GABAA受体的功能联系起来. 相似文献
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Using nystatin-perforated whole-cell recording configuration, the modulatory effect of N-methyl-D-aspartate (NMDA) on γ-aminobutyric acid (GABA)-activated whole-cell currents was investigated in neurons freshly dissociated from the rat sacral dorsal commissural nucleus (SDCN). The results showed that: (i) NMDA suppressed GABA- and muscimol (Mus)-activated currents (IGABA and IMUS), respectively in the Mg2 -free external solution containing 1 μmol/L glycine at a holding potential (VH) of -40 mV in SDCN neurons. The selective NMDA receptor antagonist, D-2-amino-5-phosphonovaleric acid (APV, 100 μmol/L), inhibited the NMDA-evoked currents and blocked the NMDA-induced suppression of IGABA; (ii) when the neurons were incubated in a Ca2 -free bath or pre-loaded with a membrane-permeable Ca2 chelator, BAPTA AM (10 nmol/L), the inhibitory effect of NMDA on IGABA disappeared. Cd2 (10 μmol/L) or La3 (30 μmol/L), the non-selective blockers of voltage-dependent calcium channels, did not affect the suppressio 相似文献
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