Vautrin J, Schaffner A E, Fontas B, Barker J L
Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
J Physiol Paris. 1993;87(1):51-73. doi: 10.1016/0928-4257(93)90024-n.
In 1952 Fatt and Katz recorded at a frog neuromuscular junction while stimulating the nerve and found "... that successive endplate potential responses varied in a step-like manner, corresponding to units of miniature endplate potentials" (J Physiol 117, 109-128). This led them to propose that fast neuromuscular transmission is 'quantal'. Quantal release is now commonly ascribed to a vesicular form of neurosecretion since vesicles have routinely been visualized in presynaptic terminals. The vesicular hypothesis (Del Castillo and Katz, 1955) assumes that quanta, or 'transmitter packets of standard size', are assembled and stored in the numerous vesicles routinely identified in micrographs of virtually all central and peripheral presynaptic nerve terminals. Simply stated, this model predicts that each one of the miniature synaptic signals (MSSs) follows from the exocytosis of one vesicle's contents. However, the time required for membrane fusion preceding exocytosis (Almers and Tse, 1990) and the variability in MSS amplitude and time course (Vautrin et al, 1992a,b) cannot readily be reconciled by a simple, exocytotic model of quantal release from preloaded vesicles. These difficulties with the original model have led us to re-evaluate MSSs generated at the classical peripheral synapse, the cholinergic neuromuscular junction of the mouse diaphragm, as well as at central synapses between embryonic hippocampal neurons mediated by gamma-aminobutyric acid (GABA). At these synapses, the release of GABA is also assumed to have classical quantal properties like peripheral acetylcholine release (Edwards et al, 1990). Our results show that at both synapses, progressive alterations in elementary signal properties can be induced in a remarkably rapid manner. The original report of preferred amplitudes and intervals in the spontaneous miniature signals (Fatt and Katz, 1952) has repeatedly been confirmed and is here incorporated into a dynamic model of fast synaptic transmission. Although MSSs exhibit variable rise-times and peak amplitudes, they can both be described in terms of synchronization of transmitter release. We have reviewed many experimental findings, which together strongly suggest that the original interpretation of Fatt and Katz (1952) regarding MSSs as reflecting the non-propagated 'neurogenic' activity of 'terminal spots' may be a useful concept to pursue since it may help to explain part of the underlying molecular basis of quantal release.(ABSTRACT TRUNCATED AT 400 WORDS)
1952年，法特和卡茨在刺激神经时记录了青蛙神经肌肉接头处的情况，发现“……连续的终板电位反应呈阶梯状变化，与微小终板电位的单位相对应”（《生理学杂志》117卷，109 - 128页）。这使他们提出快速神经肌肉传递是“量子化”的。由于在突触前终末经常能观察到囊泡，现在量子化释放通常被归因于囊泡形式的神经分泌。囊泡假说（德尔卡斯蒂略和卡茨，1955年）假定量子，即“标准大小的递质包”，是在几乎所有中枢和外周突触前神经终末的显微照片中常规识别出的众多囊泡中组装和储存的。简单来说，这个模型预测每个微小突触信号（MSS）都来自一个囊泡内容物的胞吐作用。然而，胞吐作用之前膜融合所需的时间（阿尔默斯和谢，1990年）以及MSS幅度和时程的变异性（沃特兰等人，1992年a、b），很难用一个简单的、从预装载囊泡中量子化释放的胞吐模型来解释。原始模型存在的这些困难促使我们重新评估在经典外周突触，即小鼠膈肌的胆碱能神经肌肉接头处以及由γ - 氨基丁酸（GABA）介导的胚胎海马神经元之间的中枢突触处产生的MSS。在这些突触处，GABA的释放也被假定具有像外周乙酰胆碱释放那样的经典量子特性（爱德华兹等人，1990年）。我们的结果表明，在这两种突触处，基本信号特性的渐进性改变都能以非常迅速的方式被诱导。自发微小信号中存在偏好幅度和间隔的原始报告（法特和卡茨，1952年）已被多次证实，并在此被纳入快速突触传递的动态模型中。尽管MSS表现出可变的上升时间和峰值幅度，但它们都可以用递质释放的同步性来描述。我们回顾了许多实验结果，这些结果共同强烈表明，法特和卡茨（1952年）将MSS解释为反映“终末点”的非传播性“神经源性”活动，这一解释可能是一个值得探讨的有用概念，因为它可能有助于解释量子化释放潜在分子基础的一部分。（摘要截选至400字）
