Calcium Dependence and Recovery Kinetics of Presynaptic Depression at the Climbing Fiber to Purkinje Cell Synapse
Calcium Dependence and Recovery Kinetics of Presynaptic Depression at the Climbing Fiber to Purkinje Cell Synapse
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DOI：
10.1523/jneurosci.18-16-06147.1998
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发表时间：
1998-08
期刊：
影响因子：
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通讯作者：
J. Dittman;W. Regehr
中科院分区：
文献类型：
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作者：
J. Dittman;W. Regehr
短期抑郁是一种广泛存在于无脊椎动物和脊椎动物的外周和中枢神经系统中的使用依赖性可塑性。突触强度的这种短暂降低背后的机制被认为主要是突触前容易释放的神经递质池的“耗尽”的结果，其通常以几秒的时间常数恢复。我们研究的机制和动力学的恢复抑郁症的攀缘纤维浦肯野细胞突触，显着的突触前抑郁症已被描述过。攀爬纤维非常适合研究抑郁症的恢复，因为它们几乎没有表现出任何促进作用（即使在低释放概率的条件下），这可能会在释放后的数百毫秒内掩盖抑郁症的快速恢复。我们发现，从抑郁症中恢复发生在三个动力学阶段。在24° C下，快速和中间分量可以通过时间常数为100毫秒和3秒的指数来近似。一个缓慢得多的复苏阶段也存在，但它只在长期刺激列车突出。快的组成部分，提高细胞外钙，并通过降低突触前钙消除，这表明，在短时间尺度上，抑郁症的恢复是由残余钙驱动。在定期和泊松刺激列车，从抑郁症的恢复显着加速突触前残留钙的积累，保持突触的效力，否则会耗尽可用的发射池的条件下。这代表了突触前可塑性的一种新形式，即高水平的活动调节恢复的速度以及抑郁的程度。
Short-term depression is a widespread form of use-dependent plasticity found in the peripheral and central nervous systems of invertebrates and vertebrates. The mechanism behind this transient decrease in synaptic strength is thought to be primarily the result of presynaptic “depletion” of a readily releasable neurotransmitter pool, which typically recovers with a time constant of a few seconds. We studied the mechanism and dynamics of recovery from depression at the climbing fiber to Purkinje cell synapse, where marked presynaptic depression has been described previously. Climbing fibers are well suited to studies of recovery from depression because they display little, if any, facilitation (even under conditions of low-release probability), which can obscure rapid recovery from depression for hundreds of milliseconds after release. We found that recovery from depression occurred in three kinetic phases. The fast and intermediate components could be approximated by exponentials with time constants of 100 msec and 3 sec at 24° C. A much slower recovery phase was also present, but it was only prominent during prolonged stimulus trains. The fast component was enhanced by raising extracellular calcium and was eliminated by lowering presynaptic calcium, suggesting that, on short time scales, recovery from depression is driven by residual calcium. During regular and Poisson stimulus trains, recovery from depression was dramatically accelerated by accumulation of presynaptic residual calcium, maintaining synaptic efficacy under conditions that would otherwise deplete the available transmitter pool. This represents a novel form of presynaptic plasticity in that high levels of activity modulate the rate of recovery as well as the magnitude of depression.