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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Presynaptic mechanism for phorbol ester-induced synaptic potentiation.
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Presynaptic mechanism for phorbol ester-induced synaptic potentiation.

机译：佛波酯诱导的突触增强的突触前机制。

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摘要

Phorbol ester facilitates transmitter release at a variety of synapses, and the phorbol ester-induced synaptic potentiation (PESP) is a model for presynaptic facilitation. To address the mechanism underlying PESP, we have made paired whole-cell recordings from the giant presynaptic terminal, the calyx of Held, and its postsynaptic target in the medial nucleus of the trapezoid body in rat brainstem slices. Phorbol ester potentiated EPSCs without affecting either presynaptic calcium currents or potassium currents. Protein kinase C inhibitors applied from outside or injected directly into the presynaptic terminal attenuated the PESP. Furthermore, presynaptic loading of a synthetic peptide with the sequence of the N-terminal domain of Doc2alpha interacting with Munc13-1 (Mid peptide) significantly attenuated PESP, whereas mutated Mid peptide had no effect. We conclude that the target of the presynaptic facilitatory effect of phorbol ester resides downstream of calcium influx and may involve both protein kinase C and Doc2alpha - Munc13-1 interaction.
机译：佛波酯可促进各种突触释放递质，佛波酯诱导的突触增强作用（PESP）是突触前促进的模型。为了解决PESP的潜在机制，我们在大鼠脑干切片的梯形体内侧核中，从巨大的突触前末端，Held的花萼及其突触后靶标制作了全细胞配对记录。磷酸酯增强EPSCs，而不影响突触前钙电流或钾电流。从外部施加或直接注射到突触前末端的蛋白激酶C抑制剂减弱了PESP。此外，合成肽的突触前负载与Doc2alpha的N末端结构域的序列与Munc13-1（Mid肽）相互作用会显着减弱PESP，而突变的Mid肽则没有作用。我们得出结论，佛波酯的突触前促进作用的靶标位于钙内流的下游，并且可能涉及蛋白激酶C和Doc2alpha-Munc13-1相互作用。

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