Busik J, Nakamura M, Abe Y, Shibuya I, Kanno T
Laboratory of Cellular Metabolism, National Institute for Physiological Sciences, Okazaki, Japan.
Brain Res. 1996 Nov 11;739(1-2):97-103. doi: 10.1016/s0006-8993(96)00814-1.
A large fraction of rat adrenal chromaffin cells (about 60%) shows spontaneous [Ca2+]c oscillations and spontaneous action potentials. In the present study the effects of gamma-aminobutyric acid (GABA) on the spontaneous [Ca2+]c oscillations and electrical properties of rat adrenal chromaffin cells were investigated using Fura-2 [Ca2+]c imaging and patch clamp techniques. GABA inhibited the spontaneous [Ca2+]c oscillations in a reversible manner. The effect of GABA was mimicked by the GABAA and GABAC receptor agonist, muscimol, but not by the GABAB receptor agonist, baclofen. Moreover, the effect was antagonized by the selective GABAA receptor antagonist, bicuculline. The mode of the inhibition was all-or-none, and the threshold concentration at which the inhibition occurred varied widely (50 microM to over 1 microM) from cell to cell. GABA (100 microM) elicited a transient burst of action potentials of diminished amplitude, which was followed by arrest of action potentials. Further analysis showed that GABA (100 microM) induced inward whole-cell currents in voltage-clamp experiments and produced depolarization and membrane conductance increase in current-clamp experiments. The effects appear to be due to an increase in chloride ion conductance since the degree of GABA-induced depolarization depended on the pipette [Cl-]. These results suggest that GABA, acting through GABAA receptor, may play a role in the physiological regulation of rat adrenal chromaffin cells by directly modifying the discharge of spontaneous action potentials and spontaneous [Ca2+]c oscillations.
很大一部分大鼠肾上腺嗜铬细胞（约60%）表现出自发性的胞内钙离子浓度（[Ca2+]c）振荡和自发性动作电位。在本研究中，使用Fura-2 [Ca2+]c成像和膜片钳技术研究了γ-氨基丁酸（GABA）对大鼠肾上腺嗜铬细胞自发性[Ca2+]c振荡和电特性的影响。GABA以可逆的方式抑制自发性[Ca2+]c振荡。GABAA和GABAC受体激动剂蝇蕈醇可模拟GABA的作用，但GABAB受体激动剂巴氯芬则不能。此外，选择性GABAA受体拮抗剂荷包牡丹碱可拮抗该作用。抑制模式为全或无，抑制发生的阈值浓度在不同细胞间差异很大（50微摩尔至超过1微摩尔）。GABA（100微摩尔）引发幅度减小的动作电位短暂爆发，随后动作电位停止。进一步分析表明，在电压钳实验中，GABA（100微摩尔）诱导内向全细胞电流，在电流钳实验中导致去极化和膜电导增加。这些效应似乎是由于氯离子电导增加所致，因为GABA诱导的去极化程度取决于移液管中的氯离子浓度。这些结果表明，通过GABAA受体起作用的GABA可能通过直接改变自发性动作电位的发放和自发性[Ca2+]c振荡，在大鼠肾上腺嗜铬细胞的生理调节中发挥作用。
