Bellingham M C, Walmsley B
Division of Neuroscience, The John Curtin School of Medical Research, The Australian National University, Canberra, ACT.
Neuron. 1999 May;23(1):159-70. doi: 10.1016/s0896-6273(00)80762-x.
Several distinct mechanisms may cause synaptic depression, a common form of short-term synaptic plasticity. These include postsynaptic receptor desensitization, presynaptic depletion of releasable vesicles, or other presynaptic mechanisms depressing vesicle release. At the endbulb of Held, a fast central calyceal synapse in the auditory pathway, cyclothiazide (CTZ) abolished marked paired pulse depression (PPD) by acting presynaptically to enhance transmitter release, rather than by blocking postsynaptic receptor desensitization. PPD and its response to CTZ were not altered by prior depletion of the releasable vesicle pool but were blocked by lowering external calcium concentration, while raising external calcium enhanced PPD. We conclude that a major component of PPD at the endbulb is due to a novel, transient depression of release, which is dependent on the level of presynaptic calcium entry and is CTZ sensitive.
几种不同的机制可能导致突触抑制，这是一种常见的短期突触可塑性形式。这些机制包括突触后受体脱敏、可释放囊泡的突触前耗竭或其他抑制囊泡释放的突触前机制。在听觉通路中的快速中枢花萼状突触—— Held终球，环噻嗪（CTZ）通过突触前作用增强递质释放，而非通过阻断突触后受体脱敏，消除了显著的双脉冲抑制（PPD）。可释放囊泡池预先耗竭并不会改变PPD及其对CTZ的反应，但降低细胞外钙浓度会阻断该反应，而提高细胞外钙浓度则会增强PPD。我们得出结论，Held终球处PPD的一个主要成分是由于一种新的、短暂的释放抑制，其依赖于突触前钙内流水平且对CTZ敏感。
