Calcium-channel number critically influences synaptic strength and plasticity at the active zone
How synaptic-vesicle release is controlled at the basic release structure, the active zone, is poorly understood. By performing cell-attached current and capacitance recordings predominantly at single active zones in rat calyces, we found that single active zones contained 5-218 (mean, 42) calcium c...
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| Hauptverfasser: | , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
2012 Jun 10
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| In: |
Nature neuroscience
Year: 2012, Jahrgang: 15, Heft: 7, Pages: 998-1006 |
| ISSN: | 1546-1726 |
| DOI: | 10.1038/nn.3129 |
| Online-Zugang: | Verlag, Volltext: http://dx.doi.org/10.1038/nn.3129 Verlag, Volltext: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4891200/ 
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| Verfasserangaben: | Jiansong Sheng, Liming He, Hongwei Zheng, Lei Xue, Fujun Luo, Wonchul Shin, Tao Sun, Thomas Kuner, David T Yue, and Ling-Gang Wu |
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| 245 | 1 | 0 | |a Calcium-channel number critically influences synaptic strength and plasticity at the active zone |c Jiansong Sheng, Liming He, Hongwei Zheng, Lei Xue, Fujun Luo, Wonchul Shin, Tao Sun, Thomas Kuner, David T Yue, and Ling-Gang Wu |
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| 520 | |a How synaptic-vesicle release is controlled at the basic release structure, the active zone, is poorly understood. By performing cell-attached current and capacitance recordings predominantly at single active zones in rat calyces, we found that single active zones contained 5-218 (mean, 42) calcium channels and 1-10 (mean, 5) readily releasable vesicles (RRVs) and released 0-5 vesicles during a 2-ms depolarization. Large variation in the number of calcium channels caused wide variation in release strength (measured during a 2-ms depolarization) by regulating the RRV release probability (PRRV) and the RRV number. Consequently, an action potential opened ~1-35 (mean, ~7) channels, resulting in different release probabilities at different active zones. As the number of calcium-channels determined PRRV, it critically influenced whether subsequent release would be facilitated or depressed. Regulating calcium channel density at active zones may thus be a major mechanism to yield synapses with different release properties and plasticity. These findings may explain large differences reported at synapses regarding release strength (release of 0, 1 or multiple vesicles), PRRV, short-term plasticity, calcium transients and the requisite calcium-channel number for triggering release. | ||
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