GABAA mediated afterdepolarization in pyramidal neurons from rat neocortex.
GABAA mediated afterdepolarization in pyramidal neurons from rat neocortex.
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GABAA 介导大鼠新皮质锥体神经元的后去极化。
DOI：
10.1152/jn.1997.77.2.1039
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发表时间：
1997
影响因子：
2.5
通讯作者：
Spain,WJ
中科院分区：
文献类型：
--
作者：
Cerne,R;Spain,WJ
J.西班牙.GABA介导的大鼠新皮质锥体神经元的后去极化.神经生理学杂志.77：1039-1045,1997.我们报道了在体感皮层脑片中灌流γ-氨基丁酸时，V层锥体神经元出现一种新的慢后除极。全细胞记录是从3到5周龄的大鼠脑片上肉眼识别的神经元进行的。由一串短的电流脉冲诱发的100 Hz1 S动作电位，通常伴随着缓慢的后超极化(SAHP)。灌流液中加入1 mM的γ-氨基丁酸时，≈的幅度被18 mV的sADP取代，平均持续26 S。sADP不是一个有或无的事件：它的幅度和持续时间随着诱发动作电位的增加而增加；当sADP被超极化电流阶跃打断时，其幅度和持续时间随时间和电压的变化而递增。SADP不依赖于Ca~(2+)进入细胞内：用Mn2+代替浴液中的Ca~(2+)或用20 mM双-(邻氨基苯氧基)-N，N，N‘，N’-四乙酸透析的神经元均可诱发。我们推测，sADP主要在树突中产生，因为它与小幅度动作电位的激发有关，该小幅度动作电位在体细胞膜电位通过恒定电流注入重新极化至−70 mV后继续发放。我们通过在手术切除的顶端树突的神经元中唤起sADP来检验这一假设。在这些神经元中，sADP的平均持续时间比顶端树突完整的神经元短78%，并且没有相关的小动作电位。该作用也可被蝇毒酚引起，但不能被巴氯芬引起，并可被荷包牡丹碱或印防己毒素阻断，但不能被CGp 35348阻断，这表明它是通过激活GABA受体而介导的。我们的结果表明，在GABA存在的情况下，强烈的活动导致顶树突兴奋性的持久增强，这反过来可能导致远端兴奋性突触电位的放大。
Cerne, R. and W. J. Spain.A GABAAmediated afterdepolarization in pyramidal neurons from rat neocortex.J. Neurophysiol.77: 1039–1045, 1997. We report a novel slow afterdepolarization (sADP) in layer V pyramidal neurons when brain slices from somatosensory cortex are perfused with γ-aminobutyric acid (GABA). Whole cell recordings were made from visually identified neurons in slices from 3- to 5-wk-old rats. The firing of action potentials at 100 Hz for 1 s, evoked by a train of brief current pulses, typically is followed by a slow afterhyperpolarization (sAHP). When GABA (1 mM) was applied to the perfusate, the sAHP was replaced by a sADP of ≈18 mV in amplitude, which on average lasted for 26 s. The sADP was not evoked or terminated as an all-or-none event: it grew in amplitude and duration as the number of evoked action potentials was increased; and when the sADP was interrupted with hyperpolarizing current steps, its amplitude and duration were graded in a time- and voltage-dependent manner. The sADP did not depend on Ca2+entry into the cell: it could be evoked when bath Ca2+was replaced by Mn2+or in neurons dialyzed with 20 mM bis-(o-aminophenoxy)-N,N,N′,N′-tetraacetic acid. We hypothesized that the sADP was generated predominantly in the dendrites because it was associated with the firing of small-amplitude action potentials that continued after the somatic membrane potential was repolarized to −70 mV by steady current injection. We tested this hypothesis by evoking the sADP in neurons with surgically amputated apical dendrites. In those neurons, the average duration of the sADP was 78% shorter than in neurons with an intact apical dendrite and there were no associated small action potentials. The sADP also was evoked by muscimol, but not by baclofen, and was blocked by bicuculline or picrotoxin but not by CGP 35348, indicating that it is mediated through the activation of GABAAreceptors. Our results suggest that intense activity in the presence of GABA results in a long-lasting enhancement of excitability in the apical dendrite that in turn could lead to amplification of distal excitatory synaptic potentials.
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DOI：
10.1152/jn.1995.74.5.2220
发表时间：
1995
期刊：
Journal of neurophysiology.
影响因子：
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作者：
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通讯作者：
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影响因子：
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影响因子：
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作者：
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影响因子：
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作者：
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通讯作者：
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DOI：
10.1073/pnas.86.7.2473
发表时间：
1989-04-01
影响因子：
11.1
作者：
HUGUENARD, JR;HAMILL, OP;PRINCE, DA
通讯作者：
PRINCE, DA