Journal
JOURNAL OF NEUROSCIENCE
Volume 35, Issue 26, Pages 9632-9637Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0457-15.2015
Keywords
Ca2+ sensor; spontaneous vesicle release; synaptic plasticity; VGCC
Categories
Funding
- 973 Program [2013CB835100]
- National Science Foundation of China [30970943, 31200821]
- National High-Tech RD Program [2015AA020512]
- Science and Technology Program of Yunnan Province [2013GA003]
- Beijing Institute for Brain Disorders Grant [BIBD-PXM2013_014226_07_000084]
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It is well known that voltage-gated calcium channels (VGCCs)-mediated Ca2+ influx triggers evoked synaptic vesicle release. However, the mechanisms of Ca2+ regulation of spontaneous miniature vesicle release (mini) remain poorly understood. Here we show that blocking VGCCs at the juvenile mice (C57BL/6) calyx of Held synapse failed to cause an immediate change in minis. Instead, it resulted in a significant reduction (similar to 40%) of mini frequency several minutes after the blockage. By recording VGCC activity and single vesicle fusion events directly at the presynaptic terminal, we found that minis did not couple to VGCC-mediated Ca2+ entry, arguing for a lack of direct correlation between mini and transient Ca2+ influx. Moreover, mini frequencies displayed a lower apparent Ca2+ cooperativity than those of evoked release. In agreement with this observation, abrogation of the Ca2+ sensor synaptotagmin-2 had no effect on apparent Ca2+ cooperativity of minis. Together, our study provides the first direct evidence that spontaneous minis are not mediated by transient Ca2+ signals through VGCCs and are triggered by a Ca2+-sensing mechanism that is different from the evoked release at these microdomain VGCC-vesicle coupled synapses.
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