Aroniadou V A, Maillis A, Stefanis C C
Department of Psychiatry, University of Athens, Eginition Hospital, Greece.
Neurosci Lett. 1993 Mar 5;151(1):77-80. doi: 10.1016/0304-3940(93)90050-u.
It was recently shown that induction of long-term potentiation (LTP) in the visual cortex of adult rats does not require suppression of inhibition or N-methyl-D-aspartate (NMDA) receptor activation. In the present study we examined the role of dihydropyridine-sensitive Ca2+ channels in the induction of this form of LTP. In visual cortical slices from 60 to 90-day-old rats tetanic stimulation (100 Hz 0.2 s, every 5 s for 10 min) of the white matter in the control medium or in the presence of D,L-2-amino-5-phosphonovalerate (100-200 microM) induced LTP of the field potential in layer III. Tetanic stimulation in the presence of nifedipine (50-100 microM) or nimodipine (10 microM) prevented induction of LTP in most of the slices. It appears that the known reduction of NMDA receptor activity in the mature neocortex is accompanied by a diminished role of NMDA receptors and an increased importance of voltage-gated Ca2+ channels in maintaining synaptic plasticity.
最近研究表明,成年大鼠视觉皮层中长时程增强(LTP)的诱导并不需要抑制抑制作用或N-甲基-D-天冬氨酸(NMDA)受体激活。在本研究中,我们检测了二氢吡啶敏感的Ca2+通道在这种形式的LTP诱导中的作用。在来自60至90日龄大鼠的视觉皮层切片中,在对照培养基中或存在D,L-2-氨基-5-磷酸戊酸(100 - 200 microM)的情况下,对白质进行强直刺激(100 Hz 0.2 s,每5 s一次,持续10 min)可诱导III层场电位的LTP。在硝苯地平(50 - 100 microM)或尼莫地平(10 microM)存在的情况下进行强直刺激,可阻止大多数切片中LTP的诱导。看来,成熟新皮层中已知的NMDA受体活性降低伴随着NMDA受体作用的减弱以及电压门控Ca2+通道在维持突触可塑性方面的重要性增加。