Cerne R, Spain W J
Veterans Affairs Puget Sound Health Care System, Seattle 98108, Washington, USA.
J Neurophysiol. 1997 Feb;77(2):1039-45. doi: 10.1152/jn.1997.77.2.1039.
We report a novel slow afterdepolarization (sADP) in layer V pyramidal neurons when brain slices from somatosensory cortex are perfused with gamma-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 approximately 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 GABAA receptors. 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.
我们报告了一种新的慢后去极化（sADP）现象，该现象出现在体感皮层脑片用γ-氨基丁酸（GABA）灌注时的V层锥体神经元中。全细胞记录取自3至5周龄大鼠脑片上经视觉识别的神经元。由一串短暂电流脉冲诱发的动作电位以100 Hz频率发放1 s后，通常会跟随一个慢后超极化（sAHP）。当向灌流液中加入GABA（1 mM）时，sAHP被一个幅度约为18 mV的sADP所取代，该sADP平均持续26 s。sADP并非以全或无的方式诱发或终止：其幅度和持续时间随着诱发动作电位数量的增加而增大；当用超极化电流阶跃中断sADP时，其幅度和持续时间以时间和电压依赖的方式分级变化。sADP不依赖于Ca2+进入细胞：当浴液中的Ca2+被Mn2+取代时，或者在用20 mM双（邻氨基苯氧基）-N,N,N',N'-四乙酸透析的神经元中，均可诱发sADP。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发放相关，这些小幅度动作电位在通过稳定电流注入使胞体膜电位复极化至-70 mV后仍持续存在。我们通过在手术切除顶端树突的神经元中诱发sADP来验证这一假设。在那些神经元中，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。sADP也可由蝇蕈醇诱发，但不能由巴氯芬诱发，且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GABAA受体的激活介导的。我们的结果表明，在GABA存在的情况下强烈活动会导致顶端树突兴奋性的长期增强，进而可能导致远端兴奋性突触电位的放大。
