Li Li, Wang Yang, Ma Ke-Tao, Cheng Hong-Ju, Zhao Lei, Si Jun-Qiang
Department of Physiology and Pathophysiology, Medical College Shihezi University, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2013 Mar;29(2):128-32.
To explore the modulatory effect of niflumic acid and blocker of calcium channel on the desensitization of gamma aminobutyric acid (GABA)-activated currents in dorsal root ganglion(DRG) neurons from rat.
The whole-cell patch-clamp technique was used to observe the modulatory effect of niflumic acid and blocker of calcium channel on the desensitization of GABA-activated currents in neurons freshly dissociated from rat DRG neurons.
Application of GABA (0.1-1 000 micromol/L) could induce concentration-dependent inward currents in some cells (212/223, 95.11%). GABA-(100 micromol/L) activated currents was (1.32 +/- 0.74) nA (n = 84). However, pre-application of niflumic acid (1-100 micromol/L) and nitrendipine (specific blocker of L-calcium channel)(0.1-30 micromol/L) could inhibit the GABA-activated inward current which was identified to be GABAA receptor-mediated current. The inhibitory effects of niflumic acid and nitrendipine were concentration-dependent. The suppression rate of 10 micromol/L niflumic acid and nitrendipine to GABA-activated currents were (31.60% +/- 4.87%) (n = 19) and (43.60% < or = 5.10%) (n = 5), respectively. The desensitization of GABA-activated currents had double exponential characteristic. Tau value was (14.68 +/- 5.11) s (n = 6) and (175.8 +/- 42.67) s (n = 6, r = 0.9647), respectively. Pre-application of niflumic acid (100 micromol/L) and nickel chloride (nonspecific blocker of L-calcium channel) (100 micromol/L) altered tau value of the desensitization of GABA-activated currents, tau value reduced for (4.64 +/- 2.21) s (n = 3), (43.70 +/- 14.34) s ( n = 3, r = 0.9548) and (4.64 +/- 2.21) s (n = 3), (43.70 +/- 14.34) s (n = 3, r = 0.9721).
Pre-application of niflumic acid exerts a more strong inhibitory effect on the peak value of GABA-activated current, which possibly is through blocking the calcium-activated chloride ion channel to accelerate the desensitization of GABA-activated currents.
探讨尼氟灭酸和钙通道阻滞剂对大鼠背根神经节（DRG）神经元γ-氨基丁酸（GABA）激活电流脱敏的调节作用。
采用全细胞膜片钳技术，观察尼氟灭酸和钙通道阻滞剂对新鲜分离的大鼠DRG神经元中GABA激活电流脱敏的调节作用。
应用GABA（0.1 - 1000 μmol/L）可在部分细胞（212/223，95.11%）中诱导浓度依赖性内向电流。GABA（100 μmol/L）激活的电流为（1.32 ± 0.74）nA（n = 84）。然而，预先应用尼氟灭酸（1 - 100 μmol/L）和尼群地平（L-钙通道特异性阻滞剂）（0.1 - 30 μmol/L）可抑制GABA激活的内向电流，该电流被确定为GABAA受体介导的电流。尼氟灭酸和尼群地平的抑制作用呈浓度依赖性。10 μmol/L尼氟灭酸和尼群地平对GABA激活电流的抑制率分别为（31.60% ± 4.87%）（n = 19）和（43.60% ± 5.10%）（n = 5）。GABA激活电流的脱敏具有双指数特征。时间常数（Tau值）分别为（14.68 ± 5.11）s（n = 6）和（175.8 ± 42.67）s（n = 6，r = 0.9647）。预先应用尼氟灭酸（100 μmol/L）和氯化镍（L-钙通道非特异性阻滞剂）（100 μmol/L）改变了GABA激活电流脱敏的Tau值，Tau值分别降低了（4.64 ± 2.21）s（n = 3）、（43.70 ± 14.34）s（n = 3，r = 0.9548）和（4.64 ± 2.21）s（n = 3）、（43.70 ± 14.34）s（n = 3，r = 0.9721）。
预先应用尼氟灭酸对GABA激活电流的峰值具有更强的抑制作用，这可能是通过阻断钙激活氯离子通道来加速GABA激活电流的脱敏。
