Finlayson P G, Cynader M S
Department of Ophthalmology, University of British Columbia, Vancouver, Canada.
Exp Brain Res. 1995;106(1):145-55. doi: 10.1007/BF00241364.
Synaptic depression was assessed from intracellular recordings in cortical tissue slices. Evoked postsynaptic potentials exhibited synaptic depression with an exponential or double exponential decrease (time constants: < 1-30 s) in amplitude during repetitive afferent stimulation by short trains of suprathreshold stimuli. Depressed synaptic responses with an exponential time course (time constants: 10 s-8 min) during presentation of similar short trains of stimuli every 5 or 10 s. Cortical cells recorded extracellularly in cat visual cortex show similar time constants of response decrement during adaptation to moving stripes. Postsynaptic voltage- or ion-regulated conductances and chloride conductances do not appear to be involved in synaptic depression. Input resistance changes and effects of injection of chloride indicate a lack of GABAA receptor-mediated effects. Hyperpolarizing or depolarizing neurons, and pairing polarization with afferent stimulation, also did not affect synaptic depression. This distinguishes these processes from long-term depression and long-term potentiation. Our results suggest that the most likely mechanisms of synaptic depression and adaptation in cortical cells are presynaptic decrease in transmitter release and/or receptor desensitization. Short-term postsynaptic changes may also occur after synaptic depression.
通过对皮质组织切片进行细胞内记录来评估突触抑制。在由短串阈上刺激进行重复性传入刺激期间,诱发的突触后电位表现出突触抑制,其幅度呈指数或双指数下降(时间常数:<1 - 30秒)。在每5秒或10秒呈现类似的短串刺激时,突触反应呈指数时间进程下降(时间常数:10秒 - 8分钟)。在猫视觉皮质中细胞外记录的皮质细胞在适应移动条纹时显示出类似的反应衰减时间常数。突触后电压或离子调节电导以及氯电导似乎不参与突触抑制。输入电阻变化和氯化物注射的影响表明不存在GABAA受体介导的效应。使神经元超极化或去极化,以及将极化与传入刺激配对,也不会影响突触抑制。这将这些过程与长时程抑制和长时程增强区分开来。我们的结果表明,皮质细胞中突触抑制和适应的最可能机制是突触前递质释放减少和/或受体脱敏。突触抑制后也可能发生短期突触后变化。