Physiological temperatures reduce the rate of vesicle pool depletion and short-term depression via an acceleration of vesicle recruitment
Physiological temperatures reduce the rate of vesicle pool depletion and short-term depression via an acceleration of vesicle recruitment
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DOI：
10.1523/jneurosci.3889-05.2006
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发表时间：
2006-02-01
影响因子：
5.3
通讯作者：
von Gersdorff, H
中科院分区：
文献类型：
--
作者：
Kushmerick, C;Renden, R;von Gersdorff, H
突触传递的时间和强度与温度密切相关。然而，导致短期突触可塑性的多种机制的温度依赖性尚不清楚。在这里，我们使用电压钳记录来量化hold突触花萼分泌的温度依赖性。生理温度下EPSC和微缩EPSC的振幅较大，但当温度从22-24℃跳变到35-37℃时，低频（0.05 Hz）刺激下EPSC的量子含量是恒定的。100 Hz刺激时EPSC的初始抑制程度随温度变化而不变，释放概率和囊泡池大小的估计也不变。相比之下，在100赫兹的40次刺激后，生理温度显著缓解了抑郁症，使抑郁症的恢复速度增加了两倍。突触前花萼记录显示，生理温度增加Ca2+内流增加0.5 ms和1 ms去极化导致的电容跳变。当Ca2+进入在两种温度下相等时，胞吐对短暂的去极化表现出很少的温度依赖性。然而，对于更长时间的去极化，升高的温度增加了胞吐的缓慢阶段，而不影响总体Ca2+进入或容易释放的囊泡池的大小。较高的温度也增加了突触前Ca2+电流失活的速率；然而，稳态EPSC的抑制程度大大降低。因此，我们的研究结果表明，在生理温度刺激训练中，稳态EPSCs的变化反映了更大的量子振幅和更快的突触囊泡池再填充，从而减少了长时间高频放电期间的短期抑郁。
The timing and strength of synaptic transmission is profoundly dependent on temperature. However, the temperature dependence of the multiple mechanisms that contribute to short-term synaptic plasticity is poorly understood. Here, we use voltage-clamp recordings to quantify the temperature dependence of exocytosis at the calyx of Held synapse. EPSC and miniature EPSC amplitudes were larger at physiological temperature, but quantal content during low-frequency (0.05 Hz) stimulation was constant after temperature jumps from 22-24 degrees C to 35-37 degrees C. The initial degree of EPSC depression during 100 Hz stimuli trains was unchanged with temperature, as were estimates of release probability and vesicle pool size. In contrast, physiological temperatures dramatically relieved depression measured after 40 stimuli at 100 Hz by increasing twofold the rate of recovery from depression. Presynaptic calyx recordings revealed that physiological temperature increased capacitance jumps resulting from 0.5 and 1 ms depolarizations by increasing Ca2+ influx. When Ca2+ entry was equalized at the two temperatures, exocytosis exhibited little temperature dependence for brief depolarizations. However, in response to longer depolarizations, raising temperature increased a slow phase of exocytosis, without affecting overall Ca2+ entry or the size of the readily releasable pool of vesicles. Higher temperatures also increased the rate of presynaptic Ca2+ current inactivation; nevertheless, the degree of steady-state EPSC depression was greatly reduced. Our results thus suggest that changes in steady-state EPSCs during stimulus trains at physiological temperature reflect larger quantal amplitudes and faster refilling of synaptic vesicle pools, leading to reduced short-term depression during prolonged high-frequency firing.