Akopian Abram
Department of Ophthalmology, New York University School of Medicine, NY 10016, USA.
Brain Res. 2003 Mar 28;967(1-2):235-46. doi: 10.1016/s0006-8993(03)02243-1.
Short-term plasticity of On- and Off-EPSPs, and its potential role in regulation of signal processing was studied in salamander retinal On-Off ganglion cells by whole-cell recording. Paired-pulse light stimulation resulted in a depression of On-, and an enhancement of Off-EPSCs. Recovery from depression and enhancement was exponential and complete by 20 s. Paired-pulse enhancement, but not depression, was abolished with increasing stimulus duration. Blockade of On-EPSC by L-2-amino-4-phosphonobutyrate (AP-4), an agonist at group III mGluRs, significantly increased Off-EPSCs evoked by short (<2 s) duration conditioning light stimuli, resulting in a reversal of the paired-pulse enhancement to depression. The acetylcholinesterase inhibitor eserine reduced Off-EPSC1 and increased the ratio of enhancement. An opposite effect was observed in the presence of the nACh receptor antagonist d-tubocurarine. AP-7, an antagonist of NMDA receptors attenuated the enhancement of Off-EPSCs. In current clamp mode paired-pulse stimulation resulted in a modulation of light evoked, as well as the depolarization-induced spike firing pattern of ganglion cells. The present study suggests that paired light stimulation differently modulates On and Off EPSPs, and the light-evoked spike firing pattern of On-Off ganglion cells.
通过全细胞膜片钳记录技术，研究了蝾螈视网膜开-关神经节细胞上开-关兴奋性突触后电位（On- and Off-EPSPs）的短期可塑性及其在信号处理调节中的潜在作用。双脉冲光刺激导致开-EPSCs的抑制和关-EPSCs的增强。抑制和增强的恢复呈指数形式，在20秒时完全恢复。随着刺激持续时间的增加，双脉冲增强效应消失，但双脉冲抑制效应不受影响。III组代谢型谷氨酸受体（mGluRs）激动剂L-2-氨基-4-膦酰丁酸（AP-4）对开-EPSC的阻断，显著增加了短（<2秒）持续时间条件光刺激诱发的关-EPSCs，导致双脉冲增强转变为抑制。乙酰胆碱酯酶抑制剂毒扁豆碱降低了关-EPSC1并增加了增强比率。在烟碱型乙酰胆碱受体（nACh）拮抗剂筒箭毒碱存在的情况下观察到相反的效果。NMDA受体拮抗剂AP-7减弱了关-EPSCs的增强。在电流钳模式下，双脉冲刺激导致光诱发的以及神经节细胞去极化诱导的动作电位发放模式的调制。本研究表明，双脉冲光刺激对开-关EPSPs以及开-关神经节细胞的光诱发动作电位发放模式有不同的调制作用。
