IONIC MECHANISMS OF CHOLINERGIC EXCITATION IN MAMMALIAN HIPPOCAMPAL PYRAMIDAL CELLS
IONIC MECHANISMS OF CHOLINERGIC EXCITATION IN MAMMALIAN HIPPOCAMPAL PYRAMIDAL CELLS
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DOI：
10.1016/0006-8993(82)90067-1
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发表时间：
1982-01-01
期刊：
影响因子：
2.9
通讯作者：
PRINCE, DA
中科院分区：
文献类型：
--
作者：
BENARDO, LS;PRINCE, DA
使用体外海马切片制备[豚鼠]获得CA 1海马锥体神经元的细胞内记录。ACh [乙酰胆碱]的反应进行了监测的存在下，包括Mn 2+，TTX [河豚毒素]和Ba 2+的电压依赖性电导的阻断剂。当用Mn ~（2+）阻断电压依赖性Ca ~（2+）电导和可能的间接突触前胆碱能作用时，ACh仍能引起电压敏感性的表观输入电阻（Ra）显著增加（29%），但膜电位（Vm）去极化作用不明显。当电压依赖性的Ca和Na电导分别被Mn 2+和TTX阻断时，ACh产生电压依赖性的Ra增加（31%），而没有显著的去极化。在单独含有TTX的溶液中，ACh产生Ra的电压敏感性增加（32%）以及显著的去极化（6.2 ± 0.01）。3.1 mV（SD））。乙酰胆碱短暂地阻止电导增加，随后假定的钙尖峰，这表明行动的钙激活，K-依赖的电导。施加Ba 2+（100-200 μ M）对Ra的影响模拟ACh的影响。当在BA ~（2+）存在下向神经元施加ACh时，Ra保持不变，但仍然观察到5-15 mV的Vm去极化。ACh降低电压依赖性钾电导（与延迟整流器的不同）和Ca激活的钾电导。毒蕈碱胆碱能去极化的发生是由于阻断钾传导，并介导的电压依赖性钙和钠电导，也许突触前的行动。
Intracellular recordings from CA1 hippocampal pyramidal neurons were obtained using the in vitro hippocampal slice preparation [for the guinea pig]. Responses to ACh [acetylcholine] were monitored in the presence of blockers of voltage-dependent conductances including Mn2+, TTX [tetrodotoxin] and Ba2+. When Mn2+ was used to block voltage-dependent Ca conductance and possible indirect presynaptic cholinergic actions, ACh still induced an significant voltage-sensitive increase in apparent input resistance (Ra) (29%), but only an insignificant depolarization of membrane potential (Vm). When both voltage-dependent Ca and Na conductances were blocked by application of Mn2+ and TTX, respectively, ACh produced voltage-dependent increases in Ra (31%) without significant depolarization. In solutions containing TTX alone, ACh produced voltage-sensitive increases in Ra (32%) as well as a significant depolarization (6.2 .+-. 3.1 mV (SD)). ACh transiently blocked the conductance increase which followed presumed Ca spikes, suggesting an action on the Ca-activated, K-dependent conductance. The effects of Ba2+ application (100-200 .mu.M) on Ra mimicked those of ACh. When ACh was applied to neurons in the presence of BA2+, Ra remained unchanged, although Vm depolarization of 5-15 mV was still seen. ACh decreases both a voltage-dependent K conductance (distinct form theat of the delayed rectifier) and a Ca-activated K conductance. Muscarinic cholinergic depolarization occurs as a result of blockade of K conductance and is mediated by voltage-dependent Ca and Na conductances and perhaps by presynaptic actions.