Robitaille R
Département de Physiologie, Centre de Recherche en Sciences Neurologiques, Université de Montréal, Canada.
Neuron. 1998 Oct;21(4):847-55. doi: 10.1016/s0896-6273(00)80600-5.
The ability of perisynaptic glial cells to modulate transmitter release and synaptic depression was studied at the frog neuromuscular junction (nmj). Injection of GTPgammaS in perisynaptic Schwann cells (PSCs), glial cells at this synapse, induced a reduction in the amplitude of nerve-evoked synaptic responses but had no effect on the frequency, the amplitude, or the duration of the miniature endplate currents (MEPCs). Also, paired pulse facilitation was not affected. The reduction in transmitter release was mediated by pertussis toxin-(PTX) sensitive and insensitive G proteins. Blockade of G proteins in PSCs with GDPbetaS reduced synaptic depression induced by high frequency trains of stimuli, whereas activation of G proteins occluded it. Hence, the activation by endogenous neurotransmitters of G proteins in PSCs induced a profound depression in neurotransmitter release.
在青蛙神经肌肉接头（nmj）处研究了突触周围神经胶质细胞调节递质释放和突触抑制的能力。向突触周围施万细胞（PSCs，此突触处的神经胶质细胞）中注射GTPγS，可导致神经诱发的突触反应幅度降低，但对微小终板电流（MEPCs）的频率、幅度或持续时间没有影响。此外，双脉冲易化也不受影响。递质释放的减少由百日咳毒素（PTX）敏感和不敏感的G蛋白介导。用GDPβS阻断PSCs中的G蛋白可减少高频刺激串诱导的突触抑制，而激活G蛋白则可消除这种抑制。因此，内源性神经递质激活PSCs中的G蛋白会导致神经递质释放的显著抑制。
