Xu Jianhua, Wu Ling-Gang
National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892, USA.
Neuron. 2005 May 19;46(4):633-45. doi: 10.1016/j.neuron.2005.03.024.
Repetitive nerve firings cause short-term depression (STD) of release at many synapses. Its underlying mechanism is largely attributed to depletion of a readily releasable vesicle pool (RRP) and a decreased probability of releasing a readily releasable vesicle during an action potential. Which of these two mechanisms is dominant and the mechanism that decreases the release probability remain debated. Here, we report that a decreased release probability is caused by a calcium-induced inhibition of presynaptic calcium channels, particularly P/Q-type channels at the calyx of Held in rat brainstem. This mechanism was the dominant cause of STD in a wide range of stimulation conditions, such as during 2 to 20 action potential-equivalent stimuli (AP-e) at 0.2-30 Hz and after 2 to 20 AP-e at 0.2-100 Hz. Only during > or = 100 Hz AP-e was depletion the dominant mechanism.
重复的神经放电会导致许多突触处释放的短期抑制（STD）。其潜在机制很大程度上归因于易释放囊泡池（RRP）的耗尽以及动作电位期间释放易释放囊泡的概率降低。这两种机制中哪一种占主导地位以及降低释放概率的机制仍存在争议。在此，我们报告释放概率降低是由钙诱导的突触前钙通道抑制引起的，特别是大鼠脑干中Held壶腹处的P/Q型通道。在广泛的刺激条件下，例如在0.2 - 30 Hz的2至20个动作电位等效刺激（AP - e）期间以及在0.2 - 100 Hz的2至20个AP - e之后，这种机制是STD的主要原因。只有在≥100 Hz的AP - e期间，耗尽才是主导机制。
