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Potassium conductances underlying repolarization and after-hyperpolarization in rat CA1 hippocampal interneurones.

机译:在大鼠CA1海马interneurones复极化和超极化后的钾电导。

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摘要

1. The roles of multiple potassium conductances underlying action potential repolarization and after-hyperpolarization (AHP) in visually identified st. oriens-alveus (st. O-A) inhibitory interneurones of neonatal rat CA1 hippocampal slices were determined using whole-cell patch clamp techniques. 2. 4-Aminopyridine dose-dependently prolonged the action potential repolarization. The effects of 4-AP persisted in Ca(2+)-free conditions. Action potentials evoked from hyperpolarized potentials possessed an increased rate of repolarization. These data suggest an involvement of the rapidly activating transient current, IA, in spike repolarization. 3. Action potential duration was increased in the presence of Ca(2+)-free, Cd(2+)-containing solution, iberiotoxin or 1 mM TEA. The fast component of the AHP was attenuated by these agents suggesting that the Ca(2+)-activated K+ conductance, IC, underlies both the spike repolarization and fast AHP. 4. In Ca(2+)-free conditions, TEA (> 1 mM) dose-dependently prolonged the action potential duration by blocking a late conductance in action potential repolarization, suggesting a role for the sustained current, IK. 5. The slow AHP was attenuated by Ca(2+)-free medium, apamin or the Ca2+ chelator EGTA, suggesting a role for the Ca(2+)-activated K+ conductance, IAHP. 6. We conclude that action potential repolarization and AHP of st. O-A interneurones result from the activation of pharmacologically distinct, temporally overlapping potassium conductances. These findings are discussed with reference to the voltage clamp data presented in the preceding manuscript.
机译:1.视觉识别的st。中潜在的动作电位复极化和超极化后(AHP)的多个钾电导的作用。使用全细胞膜片钳技术确定新生大鼠CA1海马切片的oriens-肺泡(st.O-A)抑制性中间神经元。 2. 4-氨基吡啶剂量依赖性地延长了动作电位的复极化。 4-AP的影响持续在无Ca(2+)的条件下。从超极化电位诱发的动作电位具有增加的复极化速率。这些数据表明,快速激活的瞬态电流IA与尖峰极化有关。 3.在无Ca(2+),含Cd(2+)的溶液,埃博毒素或1 mM TEA的存在下,动作电位的持续时间增加了。这些试剂减弱了AHP的快速成分,表明Ca(2+)激活的K +电导IC是尖峰复极化和快速AHP的基础。 4.在无Ca(2+)的条件下,TEA(> 1 mM)剂量依赖性地通过阻止动作电势复极中的晚期电导来延长动作电势的持续时间,暗示持续电流IK的作用。 5.缓慢的AHP被无Ca(2+)的培养基,木瓜蛋白酶或Ca2 +螯合剂EGTA减弱,表明Ca(2+)激活的K +电导IAHP起作用。 6.我们得出的结论是,动作电位复极化和st的AHP。 O-A中间神经元是由药理学上独特的,暂时重叠的钾电导的激活产生的。这些发现将参考上一手稿中介绍的电压钳位数据进行讨论。

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