Slow conductances in neurons from cat sensorimotor cortex in vitro and their role in slow excitability changes.
Slow conductances in neurons from cat sensorimotor cortex in vitro and their role in slow excitability changes.
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体外猫感觉运动皮层神经元的缓慢电导及其在缓慢兴奋性变化中的作用。
DOI：
10.1152/jn.1988.59.2.450
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发表时间：
1988
影响因子：
2.5
通讯作者：
Crill,WE
中科院分区：
文献类型：
--
作者：
Schwindt,PC;Spain,WJ;Foehring,RC;Chubb,MC;Crill,WE
1.使用细胞内记录和单微电极电压钳在体外切片制备中研究猫感觉运动皮层大V层神经元慢后电位的电生理学和药理学特性。这些特性用于评估后电位机制在长期兴奋性变化中的作用。 2. 在 100 Hz 下诱发 100 个尖峰后，缓慢后超极化 (sAHP) 的平均持续时间为 13.5 秒。它的时间进程最好用两个指数分量来描述，它们随着数百毫秒（早期 sAHP）和几秒（晚期 sAHP）的时间常数衰减。早期和晚期成分的振幅对膜电位敏感并提高细胞外K+浓度[(K+]o)。 3.当二价阳离子取代Ca2+时，早期sAHP降低，而晚期sAHP不受影响。我们得出结论，Ca2+ 介导的 K+ 电导是早期 sAHP 的大部分原因。在河豚毒素 (TTX) 存在的情况下，使用 1 秒电压钳步骤来引发缓慢的 AHP 或外向离子电流。这些 AHP 和电流在不含 Ca2+ 的灌注液中被消除，但它们的最长持续时间仅为几秒。因此，我们在 TTX 电压钳位期间观察到的最慢的外向电流仅对早期 sAHP 负责。 4. 通过在切片上涂抹哇巴因来检查生电 Na+-K+ 泵在晚期 sAHP 中的可能作用。哇巴因并没有选择性地降低晚期 sAHP，其作用最好通过细胞内 K+ 浓度的降低和 [K+]o 的增加来解释。 5.毒蕈碱和β-肾上腺素能激动剂减少或消除了整个（早期和晚期）sAHP。两种类型的激动剂都不影响 Ca2+ 依赖性、apamin 敏感的中等持续时间的超极化 (35)。我们得出的结论是，早期 sAHP 背后的 Ca2+ 介导的 K+ 电导和晚期 sAHP 背后的 Ca2+ 独立机制都对至少两类递质激动剂敏感。 6.我们关注毒蕈碱作用。当浓度大于 5 µM 时，整个（早期和晚期）sAHP 被缓慢后除极 (sADP) 取代。毒蕈碱通过减少潜在的外向离子电流直接降低 sAHP，并通过引起 sADP 间接降低 sAHP。 sADP 是 Ca2+ 介导的，因为它被不含 Ca2+ 的灌注液消除，但不会被 TTX 消除。 7. sAHP 和 sADP 下的离子电流会影响诱发重复放电后数秒内的兴奋性。（摘要截断为 400 字）
1. The electrophysiological and pharmacological properties of slow afterpotentials in large layer V neurons from cat sensorimotor cortex were studied in an in vitro slice preparation using intracellular recording and single-microelectrode voltage clamp. These properties were used to assess the role of afterpotential mechanisms in prolonged excitability changes. 2. The mean duration of a slow afterhyperpolarization (sAHP) was 13.5 s following 100 spikes evoked at 100 Hz. Its time course was best described by two exponential components, which decayed with time constants of several hundred milliseconds (the early sAHP) and several seconds (the late sAHP). The amplitude of both the early and late components were sensitive to membrane potential and raised extracellular K+ concentration [( K+]o). 3. The early sAHP was reduced when divalent cations were substituted for Ca2+, whereas the late sAHP was unaffected. We conclude that a Ca2+-mediated K+ conductance is responsible for much of the early sAHP. In the presence of tetrodotoxin (TTX), 1-s voltage-clamp steps were used to evoke slow AHPs or outward ionic currents. These AHPs and currents were abolished in Ca2+-free perfusate, but they had a maximum duration of only a few seconds. Thus the slowest outward currents we could observe during voltage clamp in TTX were responsible only for the early sAHP. 4. The possible role of an electrogenic Na+-K+ pump in the late sAHP was examined by applying ouabain to the slice. Ouabain did not reduce selectively the late sAHP, and its effect was best explained by a decrease in intracellular K+ concentration and an increase in [K+]o. 5. Muscarinic and beta-adrenergic agonists reduced or abolished the entire (early and late) sAHP. Neither type of agonist affected the Ca2+-dependent, apamin-sensitive medium-duration afterhyperpolarization (35). We conclude that both the Ca2+-mediated K+ conductance underlying the early sAHP and the Ca2+-independent mechanisms underlying the late sAHP are sensitive to at least two classes of transmitter agonists. 6. We focused on the muscarinic effects. When concentrations greater than 5 microM were employed, the entire (early and late) sAHP was replaced by a slow afterdepolarization (sADP). Muscarine reduced the sAHP directly by reducing the underlying outward ionic currents and indirectly by causing the sADP. The sADP was Ca2+-mediated, since it was abolished by Ca2+-free perfusate but not by TTX. 7. The ionic currents underlying the sAHP and the sADP influenced excitability for seconds following evoked repetitive firing.(ABSTRACT TRUNCATED AT 400 WORDS)