Scuri Rossana, Mozzachiodi Riccardo, Brunelli Marcello
Department of Physiology and Biochemistry "G. Moruzzi," University of Pisa, 56127 Pisa, Italy.
J Neurophysiol. 2002 Nov;88(5):2490-500. doi: 10.1152/jn.01027.2001.
We identified a new form of activity-dependent modulation of the afterhyperpolarization (AHP) in tactile (T) sensory neurons of the leech Hirudo medicinalis. Repetitive intracellular stimulation with 30 trains of depolarizing impulses at 15-s inter-stimulus interval (ISI) led to an increase of the AHP amplitude (~60% of the control). The enhancement of AHP lasted for >/=15 min. The AHP increase was also elicited when a T neuron was activated by repetitive stimulation of its receptive field. The ISI was a critical parameter for the induction and maintenance of AHP enhancement. ISI duration had to fit within a time window with the upper limit of 20 s to make the training effective to induce an enhancement of the AHP amplitude. After recovery from potentiation, AHP amplitude could be enhanced once again by delivering another training session. The increase of AHP amplitude persisted in high Mg(2+) saline, suggesting an intrinsic cellular mechanism for its induction. Previous investigations reported that AHP of leech T neurons was mainly due to the activity of the Na(+)/K(+) ATPase and to a Ca(2+)-dependent K(+) current (I(K/Ca)). In addition, it has been demonstrated that serotonin (5HT) reduces AHP amplitude through the inhibition of the Na(+)/K(+) ATPase. By blocking the I(K/Ca) with pharmacological agents, such as cadmium and apamin, we still observed an increase of the AHP amplitude after repetitive stimulation, whereas 5HT application completely inhibited the AHP increment. These data indicate that the Na(+)/K(+) ATPase is involved in the induction and maintenance of the AHP increase after repetitive stimulation. Moreover, the AHP increase was affected by the level of serotonin in the CNS. Finally, the increase of the AHP amplitude produced a lasting depression of the synaptic connection between two T neurons, suggesting that this activity-dependent phenomenon might be involved in short-term plasticity associated with learning processes.
我们在医用水蛭（Hirudo medicinalis）的触觉（T）感觉神经元中发现了一种新的与活动相关的超极化后电位（AHP）调节形式。以15秒的刺激间隔（ISI）进行30串去极化脉冲的重复细胞内刺激，导致AHP幅度增加（约为对照的60%）。AHP增强持续≥15分钟。当通过重复刺激其感受野激活T神经元时，也会引发AHP增加。ISI是诱导和维持AHP增强的关键参数。ISI持续时间必须在一个上限为20秒的时间窗口内，才能使训练有效地诱导AHP幅度增强。从增强状态恢复后，通过进行另一次训练，AHP幅度可再次增强。AHP幅度的增加在高镁（Mg²⁺）盐溶液中持续存在，表明其诱导存在内在细胞机制。先前的研究报道，水蛭T神经元的AHP主要归因于Na⁺/K⁺ ATP酶的活性以及一种钙依赖性钾电流（I(K/Ca)）。此外，已经证明血清素（5HT）通过抑制Na⁺/K⁺ ATP酶来降低AHP幅度。通过用镉和蜂毒素等药物阻断I(K/Ca)，我们在重复刺激后仍观察到AHP幅度增加，而应用5HT则完全抑制了AHP的增加。这些数据表明，Na⁺/K⁺ ATP酶参与了重复刺激后AHP增加的诱导和维持。此外，AHP的增加受中枢神经系统中血清素水平的影响。最后，AHP幅度的增加导致两个T神经元之间突触连接的持久抑制，表明这种与活动相关的现象可能参与了与学习过程相关的短期可塑性。
