Kaila K, Rydqvist B, Pasternack M, Voipio J
Department of Zoology, University of Helsinki, Finland.
J Physiol. 1992;453:627-45. doi: 10.1113/jphysiol.1992.sp019248.
A two-microelectrode current-voltage clamp and Cl(-)-selective microelectrodes were used to examine the effects of gamma-aminobutyric acid (GABA) on membrane potential, current and intracellular Cl- activity (aiCl) in the crayfish stretch receptor neurone. All experimental solutions were CO2-HCO3- free. 2. GABA (500 microM) produced a mono- or biphasic depolarization (amplitude < or = 10 mV), often with a prominent initial depolarizing component followed by a transient shift to a more negative level. In some neurones, an additional depolarizing phase was seen upon washout of GABA. Receptor desensitization, being absent, played no role in the multiphasic actions of GABA. 3. The pronounced increase in membrane conductance evoked by GABA (500 microM) was associated with an increase in aiCl which indicates that the depolarizing action was not due to a current carried by Cl- ions. 4. The currents activated by GABA under voltage clamp conditions were inwardly directed when recorded at the level of the resting membrane potential, and they often revealed a biphasic character. The reversal potential of peak currents activated by pulses of 500 microM-GABA (EGABA) was 9-12 mV more positive than the reversal potential of the simultaneously measured net Cl- flux (ECl). ECl was 2-7 mV more negative than the resting membrane potential. 5. EGABA (measured using pulses of 500 microM-GABA) was about 10 mV more positive than the reversal potential of the current activated by 500 microM-muscimol, a GABA agonist that is a poor substrate of the Na(+)-dependent GABA uptake system. 6. In the absence of Na+, the depolarization and inward current caused by 500 microM-GABA were converted to a hyperpolarization and to an outward current. Muscimol produced an immediate outward current both in the presence and absence of Na+. 7. Following block of the inhibitory channels by picrotoxin (100-200 microM), the depolarizing effect of 500 microM-GABA was enhanced and the transient hyperpolarizing shifts were abolished. 8. In the presence of picrotoxin, GABA (> or = 2 microM) produced a concentration-dependent monophasic inward current which had a reversal potential of +30 to +60 mV. This current was inhibited in the absence of Na+ and by the GABA uptake blocker, nipecotic acid. Unlike the channel-mediated current, the picrotoxin-insensitive current was activated without delay also at low (2-10 microM) concentrations of GABA.(ABSTRACT TRUNCATED AT 400 WORDS)
使用双微电极电流-电压钳和Cl(-)选择性微电极来研究γ-氨基丁酸（GABA）对小龙虾牵张感受器神经元膜电位、电流和细胞内Cl-活性（aiCl）的影响。所有实验溶液均不含CO2-HCO3-。2. GABA（500微摩尔）产生单相或双相去极化（幅度≤10毫伏），通常有一个明显的初始去极化成分，随后短暂转变为更负的水平。在一些神经元中，洗脱GABA后会出现额外的去极化阶段。由于不存在受体脱敏，其在GABA的多相作用中不起作用。3. GABA（500微摩尔）引起的膜电导显著增加与aiCl增加相关，这表明去极化作用不是由Cl-离子携带的电流引起的。4. 在电压钳条件下，GABA激活的电流在静息膜电位水平记录时是内向的，并且它们通常表现出双相特征。由500微摩尔-GABA脉冲激活的峰值电流的反转电位（EGABA）比同时测量的净Cl-通量的反转电位（ECl）更正9-12毫伏。ECl比静息膜电位负2-7毫伏。5. EGABA（使用500微摩尔-GABA脉冲测量）比由500微摩尔蝇蕈醇激活的电流的反转电位更正约10毫伏，蝇蕈醇是一种GABA激动剂，是Na(+)依赖性GABA摄取系统的不良底物。6. 在没有Na+的情况下，500微摩尔-GABA引起的去极化和内向电流转变为超极化和外向电流。蝇蕈醇在有和没有Na+的情况下都会立即产生外向电流。7. 在用苦味毒（100-200微摩尔）阻断抑制性通道后，500微摩尔-GABA的去极化作用增强，短暂的超极化转变被消除。8. 在存在苦味毒的情况下，GABA（≥2微摩尔）产生浓度依赖性单相内向电流，其反转电位为+30至+60毫伏。该电流在没有Na+和GABA摄取阻断剂尼克酸的情况下受到抑制。与通道介导的电流不同，苦味毒不敏感电流在低（2-10微摩尔）浓度的GABA下也能立即被激活。（摘要截短至400字）
