Ogata N, Inoue M, Matsuo T
Department of Pharmacology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Synapse. 1987;1(1):62-9. doi: 10.1002/syn.890010109.
Properties of membrane K+ conductances induced by baclofen and gamma-aminobutyric acid (GABA) in the hippocampus were investigated by using guinea-pig brain slices. Baclofen hyperpolarized the membrane and decreased the input resistance of pyramidal cells through the activation of a membrane K+ conductance. GABA caused a biphasic response in pyramidal cells, consisting of hyperpolarizing and depolarizing components. Combined application of picrotoxin and bicuculline eliminated the major part of the depolarizing component of the biphasic response and produced a relatively pure hyperpolarizing response which was also mediated by an increase in K+ conductance. The K+ conductance change induced by baclofen showed prominent inward rectification. However, the K+ conductance induced by GABA did not show an obvious rectifying property. The K+ conductance activated by baclofen was strongly antagonized by a low concentration (5 x 10(-6) M) of 4-aminopyridine (4-AP). In contrast, the K+ conductance activated by GABA was insensitive to 4-AP even at a high concentration of 10(-3) M. The slow inhibitory postsynaptic potential (slow i.p.s.p.) evoked by stimulation of the mossy fibres was totally suppressed by a low concentration of baclofen (5 x 10(-6) M). Whereas GABA (10(-3) M) decreased the amplitude of the slow i.p.s.p., the reduction of the amplitude was proportional to the decrease in the amplitude of the electrotonic potentials produced by constant inward current injections. These results suggest that the hyperpolarizations induced by GABA and baclofen may be generated by K+ conductances of different kinetic and pharmacologic properties.
运用豚鼠脑片研究了巴氯芬和γ-氨基丁酸（GABA）在海马体中诱导产生的膜钾离子电导特性。巴氯芬使膜超极化，并通过激活膜钾离子电导降低锥体细胞的输入电阻。GABA在锥体细胞中引起双相反应，包括超极化和去极化成分。联合应用苦味毒和荷包牡丹碱消除了双相反应去极化成分的大部分，产生了相对纯粹的超极化反应，该反应也是由钾离子电导增加介导的。巴氯芬诱导的钾离子电导变化表现出明显的内向整流特性。然而，GABA诱导的钾离子电导未表现出明显的整流特性。低浓度（5×10⁻⁶ M）的4-氨基吡啶（4-AP）强烈拮抗巴氯芬激活的钾离子电导。相反，即使在高浓度10⁻³ M时，GABA激活的钾离子电导对4-AP也不敏感。低浓度的巴氯芬（5×10⁻⁶ M）完全抑制了苔藓纤维刺激诱发的慢抑制性突触后电位（慢IPSP）。而GABA（10⁻³ M）降低了慢IPSP的幅度，幅度的降低与恒定内向电流注入产生的电紧张电位幅度的降低成比例。这些结果表明，GABA和巴氯芬诱导的超极化可能由具有不同动力学和药理学特性的钾离子电导产生。
