Sah P, Bekkers J M
Neuroscience Group and the Discipline of Physiology, University of Newcastle, New South Wales, Australia.
J Neurosci. 1996 Aug 1;16(15):4537-42. doi: 10.1523/JNEUROSCI.16-15-04537.1996.
Trains of action potentials in hippocampal pyramidal neurons are followed by a prolonged afterhyperpolarization (AHP) lasting several seconds, which is attributable to the activation of a slow calcium-activated potassium current ((sI)AHP). Here we examine the location of (sI)AHP on CA1 pyramidal neurons by comparing it with two GABAergic inhibitory postsynaptic currents (IPSCs) with known somatic and dendritic locations. Whole-cell patch-clamp recordings were made for CA1 pyramidal neurons in acute hippocampal slices. Stepping the membrane potential at the peak of (sI)AHP produced a relaxation ("switchoff") of the AHP current with a time constant of 7.4 +/- 0.4 msec (mean +/- SEM). The switchoff time constants for somatic and dendritic GABAA IPSCs were 3.5 +/- 0.5 msec and 8.8 +/- 0.3 msec, respectively. This data, together with cable modeling, indicates that active (sI)AHP channels are distributed over the proximal dendrites within approximately 200 micrometers of the soma. Excitatory postsynaptic potentials (EPSPs) evoked in stratum (s.) radiatum had their amplitudes shunted more by the AHP than did EPSPs evoked in s. oriens, suggesting that active AHP channels are restricted to the apical dendritic tree. Blockade of the AHP during a tetanus, which in control conditions elicited a decremental short-term potentiation (STP), converted STP to long-term potentiation (LTP). Thus, activation of the AHP increases the threshold for induction of LTP. These results suggest that in addition to its established role in spike frequency adaptation, the AHP works as an adjustable gain control, variably hyperpolarizing and shunting synaptic potentials arising in the apical dendrites.
海马锥体神经元的动作电位串之后会跟随一个持续数秒的延长的超极化后电位（AHP），这归因于一种缓慢的钙激活钾电流（（sI）AHP）的激活。在这里，我们通过将（sI）AHP与两种已知位于胞体和树突的GABA能抑制性突触后电流（IPSCs）进行比较，来研究其在CA1锥体神经元上的位置。对急性海马脑片中的CA1锥体神经元进行全细胞膜片钳记录。在（sI）AHP峰值处调节膜电位会使AHP电流出现一个具有7.4±0.4毫秒（平均值±标准误）时间常数的松弛（“关闭”）。胞体和树突GABAA IPSCs的关闭时间常数分别为3.5±0.5毫秒和8.8±0.3毫秒。这些数据，连同电缆模型，表明活跃的（sI）AHP通道分布在距离胞体约200微米范围内的近端树突上。在辐射层诱发的兴奋性突触后电位（EPSPs）比在原层诱发的EPSPs受到AHP的分流作用更大，这表明活跃的AHP通道局限于顶端树突。在强直刺激期间阻断AHP，在对照条件下会引发递减的短期增强（STP），而此时会将STP转变为长期增强（LTP）。因此，AHP的激活增加了LTP诱导的阈值。这些结果表明，除了其在动作电位频率适应中已确定的作用外，AHP还作为一种可调节的增益控制，可变地超极化并分流顶端树突中产生的突触电位。
