کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4352272 | 1298103 | 2011 | 8 صفحه PDF | دانلود رایگان |

Neuronal firing activity controls protein function and dynamically remodels synaptic efficacy. Exocytosis is triggered and regulated by Ca2+, which enters through voltage-gated Ca2+ (CaV) channels and diffuses into the presynaptic terminal accompanying action potential firings. Residual Ca2+ is sensed by Ca2+-binding proteins; among other potential actions, it mediates time- and space-dependent synaptic facilitation and depression via effects on CaV2 channel gating and vesicle replenishment in the readily releasable pool (RRP). Mitochondria are also associated with short-term synaptic plasticity due to a sufficient ATP supply for vesicle mobilization into the RRP. Mitochondria-deficient synapses with impaired anterograde transport of mitochondria in neuronal processes show defects in presynaptic short-term plasticity.
Journal: Neuroscience Research - Volume 70, Issue 1, May 2011, Pages 16–23