A calcium-activated hyperpolarization follows repetitive firing in hippocampal neurons.
A calcium-activated hyperpolarization follows repetitive firing in hippocampal neurons.
复制标题
海马神经元重复放电后会出现钙激活的超极化。
作者：
J. Hotson;D. Prince
1.体外研究海马CA 1区神经元在电流诱导的重复放电后出现持续时间较长的后超极化（AHP）。在AHP过程中，膜斜率电导增加10-25%，这表明它可能是由K+或Cl-的电导增加介导的。2.细胞内Cl-离子导入不改变AHP，但减弱IPSP。相反，Ba 2+，一种可以降低K+电导的阳离子，消除了AHP，但不是IPSP。这些结果表明，AHP是由一个持久的增加电导K+，是不同于IPSP。3. Mn ~（2+）是一种Ca ~（2+）通道阻滞剂，可消除AHP。相比之下，AHP在Na+通道阻断剂河豚毒素（TTX）的存在下持续存在，并且似乎与TTX抗性“Ca 2+尖峰”暂时相关。“可以得出结论，AHP可能是由Ca 2+内流激活的。4.这些观察结果表明，AHP可能是由Ca 2+激活的K+电流产生的。由Ca 2+进入产生的细胞去极化和由Ca 2+激活的K+电流产生的复极化之间的平衡似乎在某些哺乳动物皮层神经元中起控制兴奋性的作用，就像在软体动物神经元中一样。这种平衡被Ba 2+破坏，在海马神经元中产生自发的膜电位振荡和周期性爆发放电。Ca 2+去极化的幅度和持续时间的增加和/或Ca 2+激活的K+介导的复极化的减少可能是导致哺乳动物皮层神经元自发性癫痫样爆发的机制。
1. A long-lasting afterhyperpolarization (AHP) follows current-induced repetitive firing in hippocampal CA1 neurons studied in vitro. A 10-25% increase in membrane slope conductance occurs during the AHP, suggesting that it may be mediated by an increased conductance to either K+ or Cl-. 2. Intracellular Cl- iontophoresis does not alter the AHP but does attenuate the IPSP. In contrast Ba2+, a cation that can decrease K+ conductance, eliminates the AHP but not the IPSP. These findings suggest the AHP is produced by a long-lasting increased conductance to K+, and is distinct from the IPSP. 3. Mn2+, a Ca2+-channel blocker, eliminates the AHP. In comparison, the AHP persists in the presence of the Na+-channel blocker, tetrodotoxin (TTX), and appears to be temporally associated with TTX-resistant "Ca2+ spikes." It is concluded that AHP is probably activated by Ca2+ influx. 4. These observations indicate that the AHP may be produced by a Ca2+ activated K+ current. A balance between cellular depolarization produced by Ca2+ entry and repolarization generated by a Ca2+-activated K+ current appears to operate to control excitability in some mammalian cortical neurons as it does in molluscan neurons. Disruption of this balance by Ba2+ produces spontaneous membrane-potential oscillations and recurrent burst firing in hippocampal neurons. Increases in the magnitude and duration of Ca2+ depolarization and/or decreases in the Ca2+-activated, K+-mediated repolarization may be mechanisms that lead to spontaneous, epileptiform bursting in mammalian cortical neurons.