Krampfl K, Lepier A, Jahn K, Franke C, Bufler J
Department of Neurology, Technical University Munich, Germany.
Neurosci Lett. 1998 Nov 13;256(3):143-6. doi: 10.1016/s0304-3940(98)00767-8.
Recombinant gamma-aminobutyric acid (GABA(A)) receptor channels containing alpha1beta2gamma2-subunits were transiently expressed in HEK293 cells. Modulation by diazepam (DZ) was investigated using the patch-clamp technique with a device for ultra-fast solution exchange. GABA activated Cl(-)-currents were potentiated when DZ > 0.1 microM was added to non-saturating concentrations of GABA (< 0.1 mM GABA). Maximal potentiation of the peak current amplitude by a factor of 2.5 was observed when 1 microM DZ was added to the test-solution. Deactivation of GABA-activated currents after the end of GABA pulses was best fitted with two time constants. After application of DZ + GABA, increase of time constants of deactivation was measured. It was independent on GABA concentration. We conclude that prolongation of deactivation after application of GABA + DZ may be an important mechanism of the modulatory action of DZ at GABA(A) receptor channels.
含有α1β2γ2亚基的重组γ-氨基丁酸（GABA(A)）受体通道在人胚肾293（HEK293）细胞中瞬时表达。使用具有超快速溶液交换装置的膜片钳技术研究了地西泮（DZ）的调节作用。当在非饱和浓度的GABA（<0.1 mM GABA）中加入DZ>0.1 μM时，GABA激活的Cl(-)电流增强。当在测试溶液中加入1 μM DZ时，观察到峰值电流幅度最大增强了2.5倍。GABA脉冲结束后，GABA激活电流的失活最适合用两个时间常数来拟合。应用DZ + GABA后，测量到失活时间常数增加。它与GABA浓度无关。我们得出结论，应用GABA + DZ后失活的延长可能是DZ对GABA(A)受体通道调节作用的重要机制。
