MULTIPLE POTASSIUM CONDUCTANCES AND THEIR FUNCTIONS IN NEURONS FROM CAT SENSORIMOTOR CORTEX INVITRO
MULTIPLE POTASSIUM CONDUCTANCES AND THEIR FUNCTIONS IN NEURONS FROM CAT SENSORIMOTOR CORTEX INVITRO
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DOI：
10.1152/jn.1988.59.2.424
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发表时间：
1988-02-01
影响因子：
2.5
通讯作者：
CRILL, WE
中科院分区：
文献类型：
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作者：
SCHWINDT, PC;SPAIN, WJ;CRILL, WE
1.采用猫感觉运动皮层的离体切片，研究了大V层神经元的钾电导。直接使用单微电极电压钳和间接通过诱发单个或多个峰电位并记录峰电位复极化和随后的后超极化（AHPs）来研究K+电流的动力学和药理学敏感性。2.一个快速衰减后超极化（fAHP）和随后的中期持续时间后超极化（mAHP）遵循一个单一的尖峰。当以快速诱发多个尖峰时，mAHP的幅度和持续时间增加（例如，100 Hz），和一个较慢的后超极化（sAHP）出现后，只有持续重复射击。3.所有的AHPs降低膜电位超极化和提高细胞外K+浓度，这表明它们是由增加K+电导。只有mAHP和sAHP在钾平衡电位的估计值（-100 mV）处发生逆转，而fAHP的平均逆转电位与静息电位的平均值（-71 mV）几乎相同。4.研究了锋电位复极、fAHP和mAHP的机制。两个快速激活外向电流，快速失活电流和缓慢失活延迟整流，检测电压钳。两种电流均被四乙基铵（TEA）迅速降低。二价阳离子取代钙离子后，快速瞬态电流缓慢降低（通过一种与阻断钙离子通道无关的机制），而延迟整流不受影响。5.尖峰持续时间增加，fAHP被取消，只有通过阻断剂，减少了快速外向电流。细胞外和细胞内TEA的作用相似。TEA和无钙灌流液的效果是相加的，类似于细胞内Cs+的效果。添加apamin、d-管箭毒或Cd 2+无效。我们的结论是，这两个快速外向电流反映了主要负责尖峰复极和fAHP的动力学分离的K+电导。6.电压钳研究发现两个额外的外向电流，这是持久的和Ca 2+介导的。每种电流激活和失活缓慢，但一种组分的动力学比另一种慢约10倍。这些电流的衰减产生了类似于mAHP和早期sAHP的AHP。7.无论是mAHP还是sAHP都没有被TEA降低。当二价阳离子取代Ca 2+或当Cd 2+，apamin，或d-tubocurare被添加时，降低mAHP。（400字处截断摘要）
1. Potassium conductances were studied in large layer V neurons using an in vitro slice preparation of cat sensorimotor cortex. The kinetics and pharmacological sensitivity of K+ currents were studied directly using single microelectrode voltage clamp and indirectly by evoking single or multiple spikes and recording the spike repolarization and subsequent afterhyperpolarizations (AHPs). 2. A fast-decaying afterhyperpolarization (fAHP) and a subsequent medium-duration afterhyperpolarization (mAHP) followed a single spike. The amplitude and duration of the mAHP increased when multiple spikes were evoked at a fast rate (e.g., 100 Hz), and a slower afterhyperpolarization (sAHP) appeared only after sustained repetitive firing. 3. All AHPs were reduced by membrane potential hyperpolarization and raised extracellular K+ concentration, suggesting they were caused by an increased K+ conductance. Only the mAHP and sAHP reversed at the estimated value of potassium equilibrium potential (-100 mV), whereas the mean reversal potential of the fAHP was nearly identical to the mean value of resting potential (-71 mV). 4. Mechanisms underlying spike repolarization, the fAHP, and the mAHP were investigated. Two rapidly activating outward currents, a fast-inactivating current and a slowly inactivating delayed rectifier, were detected by voltage clamp. Both currents were reduced rapidly by tetraethylammonium (TEA). The fast transient current was reduced slowly after divalent cations were substituted for Ca2+ (through a mechanism unrelated to blockade of Ca2+ channels), whereas the delayed rectifier was unaffected. 5. Spike duration was increased and the fAHP was abolished only by blocking agents that reduced the fast outward currents. Effects of extracellular and intracellular TEA were similar. Effects of TEA and Ca2+-free perfusate were additive and resembled the effects of intracellular Cs+. The addition of apamin, d-tubocurare, or Cd2+ was ineffective. We conclude that the two fast outward currents reflect pharmacologically and kinetically separate K+ conductances that are primarily responsible for spike repolarization and the fAHP. 6. Voltage-clamp studies revealed two additional outward currents, which were persistent and Ca2+-mediated. Each current activated and deactivated slowly, but the kinetics of one component were approximately 10 times slower than the other. The decay of these currents gave rise to AHPs resembling the mAHP and the early sAHP. 7. Neither the mAHP nor the sAHP was reduced by TEA. The mAHP was reduced when divalent cations were substituted for Ca2+ or when Cd2+, apamin, or d-tubocurare were added.(ABSTRACT TRUNCATED AT 400 WORDS)