Suzuki T, Kusano K
J Neurobiol. 1978 Sep;9(5):367-92. doi: 10.1002/neu.480090504.
The mechanisms of three types of hyperpolarizing electrogenesis in hamster submandibular ganglion cells were analyzed with intracellular microelectrodes. These included (1) spike-induced hyperpolarizing afterpotential (S-HAP), (2) spontaneous transient hyperpolarizing potential (HP), and (3) the hyperpolarizing (H) phase of postsynaptic potential (PSP). Most of these hyperpolarizing potentials were due to conductance increases and reversed polarity at membrane potential (Em) between -70 and -85 mV, which was close to the K-equilibrium potential. The average resting potential of ganglion cells was -53 mV. Action potential overshoot increased slightly in high [Ca2+]0 and decreased in low [Ca2+]0. In most neurons action potentials were completely suppressed by 10(-7)-M tetrodotoxin (TTX). The S-HAP has an initial component due to delayed rectification and a late component. The late component is enhanced by increasing [Ca2+]0, or by applying Ca-ionophore (A23187), TEA, caffeine, or dibutyryl cyclic (DBc-) AMP; it is suppressed by decreasing [Ca2+]0, or by applying Mn2+. Perfusion with Cl--free saline reduced membrane potential slightly but did not modify the S-HAP. Depolarizing pulses also induced hyperpolarizing afterpotential (D-HAP), similar to the S-HAP. Spontaneous transient HPs occurred in some neurons at irregular intervals. HPs were insensitive to TTX but were suppressed by Mn2+. Caffeine induced low frequency rhythmic HPs in many neurons, often alternating with periods of repetitive spiking. The PSP was a monophasic depolarizing (D-) potential in some neurons, but in others the D-phase was followed by a small H-phase. Perfusion with A23187, caffeine or DBc-AMP increased the H-phase of the PSP. Perfusion with K+-free saline or treatment with 10(-5)M ouabain did not abolish the H-phase of PSPs. These membrane potential-dependent phenomena appear to be induced mainly by Ca-mediated K-conductance increases. This mechanism contributes to the regulation of low-frequency repetitive firing in submandibular ganglion cells.
用细胞内微电极分析了仓鼠下颌下神经节细胞中三种超极化电发生机制。这些机制包括：（1）锋电位诱发的超极化后电位（S-HAP），（2）自发性瞬态超极化电位（HP），以及（3）突触后电位（PSP）的超极化（H）相。这些超极化电位大多是由于电导增加，且在膜电位（Em）为-70至-85 mV之间时极性反转，该电位接近钾平衡电位。神经节细胞的平均静息电位为-53 mV。动作电位的超射在高[Ca2+]0时略有增加，在低[Ca2+]0时降低。在大多数神经元中，动作电位被10（-7）-M河豚毒素（TTX）完全抑制。S-HAP有一个由延迟整流引起的初始成分和一个后期成分。后期成分通过增加[Ca2+]0，或应用钙离子载体（A23187）、TEA、咖啡因或二丁酰环（DBc-）AMP而增强；通过降低[Ca2+]0，或应用Mn2+而受到抑制。用无Cl-生理盐水灌注可使膜电位略有降低，但不改变S-HAP。去极化脉冲也诱发超极化后电位（D-HAP），类似于S-HAP。自发性瞬态HPs在一些神经元中以不规则的间隔出现。HPs对TTX不敏感，但被Mn2+抑制。咖啡因在许多神经元中诱发低频节律性HPs，常与重复放电期交替出现。PSP在一些神经元中是单相去极化（D-）电位，但在另一些神经元中，D相之后是一个小的H相。用A23187、咖啡因或DBc-AMP灌注可增加PSP的H相。用无K+生理盐水灌注或用10（-5）M哇巴因处理并不能消除PSP的H相。这些膜电位依赖性现象似乎主要是由钙介导的钾电导增加所诱发。这种机制有助于调节下颌下神经节细胞中的低频重复放电。
