Misgeld U, Deisz R A, Dodt H U, Lux H D
Science. 1986 Jun 13;232(4756):1413-5. doi: 10.1126/science.2424084.
Hippocampal inhibitory postsynaptic potentials are depolarizing in granule cells but hyperpolarizing in CA3 neurons because the reversal potentials and membrane potentials of these cells differ. Here the hippocampal slice preparation was used to investigate the role of chloride transport in these inhibitory responses. In both cell types, increasing the intracellular chloride concentration by injection shifted the reversal potential of these responses in a positive direction, and blocking the outward transport of chloride with furosemide slowed their recovery from the injection. In addition, hyperpolarizing and depolarizing inhibitory responses and the hyperpolarizing and depolarizing responses to the inhibitory neurotransmitter gamma-aminobutyric acid decreased in the presence of furosemide. These effects of furosemide suggest that the internal chloride activity of an individual hippocampal neuron is regulated by two transport processes, one that accumulates chloride and one that extrudes chloride.
海马体抑制性突触后电位在颗粒细胞中是去极化的，但在CA3神经元中是超极化的，因为这些细胞的反转电位和膜电位不同。在这里，使用海马脑片制备来研究氯离子转运在这些抑制性反应中的作用。在这两种细胞类型中，通过注射增加细胞内氯离子浓度会使这些反应的反转电位向正向移动，而用呋塞米阻断氯离子的外向转运则会减缓它们从注射中的恢复。此外，在呋塞米存在的情况下，超极化和去极化抑制性反应以及对抑制性神经递质γ-氨基丁酸的超极化和去极化反应都会降低。呋塞米的这些作用表明，单个海马神经元的细胞内氯离子活性受两种转运过程调节，一种积累氯离子，另一种排出氯离子。
