Vyshedskiy A, Lin J W
Department of Biology, Boston University, Boston, Massachusetts 02215, USA.
J Neurophysiol. 1997 Oct;78(4):1791-9. doi: 10.1152/jn.1997.78.4.1791.
A presynaptic voltage-control method was used to study synaptic facilitation at the inhibitory neuromuscular synapse of the crayfish opener muscle. The expression of the F2 component of facilitation, monitored 150 ms after a conditioning stimulus, was examined by systematically changing the duration of the presynaptic test pulse. (Test pulses in all experiments were depolarized to 0 mV.) Control and facilitated inhibitory postsynaptic potentials (IPSPs) exhibited identical time courses when test pulse duration was brief (approximately 2 ms). When the duration of the test pulse was increased beyond 2 ms, the transmitter release time course shifted to an earlier point in time during facilitation. Meanwhile, the increase in total transmitter release, measured from inhibitory postsynaptic conductance (IPSG) area (total release), became less pronounced with increasing duration of the test pulse. With a 20-ms test pulse, facilitation did not cause any detectable change in total release but the half-maximal point of the facilitated IPSG shifted by 3 ms (release shift). This change in release kinetics was not associated with a decrease in minimal synaptic delay. Furthermore, the relationship between total release and presynaptic pulse duration suggested that the transmitter release activated by a 20-ms pulse can be defined as a distinct component of continuous transmitter release (early component). The facilitation process accelerated the release kinetics of the early component but did not modify its total transmitter content. To test the hypothesis that the release shift is indeed mediated by the same mechanism that increases IPSP amplitude during facilitation, we investigated the correlation between the release shift and IPSP amplitude change. The two parameters were significantly correlated when the magnitude of facilitation was changed 1) during the decay of facilitation and 2) by varying the strength of the conditioning stimulus. The experimental approach reported here provides two new physiological parameters, release shift and total release, for the analysis of synaptic facilitation.
采用突触前电压控制方法研究小龙虾开肌抑制性神经肌肉突触处的突触易化。在条件刺激后150毫秒监测易化的F2成分的表达，通过系统改变突触前测试脉冲的持续时间来进行检测。（所有实验中的测试脉冲均去极化至0 mV。）当测试脉冲持续时间较短（约2毫秒）时，对照和易化的抑制性突触后电位（IPSP）呈现相同的时间进程。当测试脉冲持续时间增加到超过2毫秒时，递质释放的时间进程在易化期间提前。同时，从抑制性突触后电导（IPSG）面积测量的总递质释放增加量，随着测试脉冲持续时间的增加而变得不那么明显。使用20毫秒的测试脉冲时，易化并未导致总释放有任何可检测到的变化，但易化的IPSG的半数最大值点提前了3毫秒（释放偏移）。这种释放动力学的变化与最小突触延迟的减少无关。此外，总释放与突触前脉冲持续时间之间的关系表明，由20毫秒脉冲激活的递质释放可被定义为连续递质释放的一个独特成分（早期成分）。易化过程加速了早期成分的释放动力学，但并未改变其总递质含量。为了检验释放偏移确实由易化期间增加IPSP幅度的相同机制介导这一假设，我们研究了释放偏移与IPSP幅度变化之间的相关性。当易化程度在1）易化衰减期间和2）通过改变条件刺激强度而改变时，这两个参数显著相关。这里报道的实验方法为突触易化分析提供了两个新的生理参数，即释放偏移和总释放。
