Vautrin J, Schaffner A E, Barker J L
Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Neurosci Lett. 1993 Aug 20;158(2):125-9. doi: 10.1016/0304-3940(93)90245-g.
Different mechanisms of neurotransmitter secretion at synapses have been ascribed to quantal, transient signals [4-9] and to continuous, tonic activity [11, 21, 25]. Quantal transmission is imputed to be the release of transmitter packets, or quanta [6], assembled and stored in vesicles present in presynaptic terminals [2,8]. We report that 300 microM Zn2+ rapidly transformed tonic Cl- conductance mediated by the transmitter gamma-aminobutyric acid (GABA) into transient synaptic-like signals. After addition of Zn2+, the size of the elementary fluctuations in the Cl- current progressively increased while randomly activated Cl- channel kinetics remained unchanged and accounted for the bi-exponential time course of average transient decay. The results suggest that Zn2+ rapidly transforms tonic GABA secretion into quantal-like transient release.
突触处神经递质分泌的不同机制已归因于量子化的瞬态信号[4 - 9]和持续性的紧张性活动[11, 21, 25]。量子化传递被认为是由存在于突触前终末的囊泡中组装并储存的递质包(即量子)的释放[6]。我们报告,300微摩尔的锌离子(Zn2+)迅速将由递质γ-氨基丁酸(GABA)介导的紧张性氯离子电导转化为类似突触的瞬态信号。加入Zn2+后,氯离子电流中基本波动的大小逐渐增加,而随机激活的氯离子通道动力学保持不变,并解释了平均瞬态衰减的双指数时间进程。结果表明,Zn2+迅速将紧张性GABA分泌转化为类似量子化的瞬态释放。