Journal
NEURON
Volume 90, Issue 5, Pages 984-999Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2016.04.038
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Funding
- Swiss National Science Foundation (SNSF) [310030B_156934/1]
- Deutsche Forschungsgemeinschaft (SPP) [1608-SCHN 451/5-1]
- Swiss National Science Foundation (SNF) [310030B_156934] Funding Source: Swiss National Science Foundation (SNF)
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Various Synaptotagmin (Syt) isoform genes are found in mammals, but it is unknown whether Syts can function redundantly in a given nerve terminal, or whether isoforms can be switched during the development of a nerve terminal. Here, we investigated the possibility of a developmental Syt isoform switch using the calyx of Held as a model synapse. At mature calyx synapses, fast Ca2+-driven transmitter release depended entirely on Syt2, but the release phenotype of Syt2 knockout (KO) mice was weaker at immature calyces, and absent at pre-calyceal synapses early postnatally. Instead, conditional genetic inactivation shows that Syt1 mediates fast release at pre-calyceal synapses, as well as a fast release component resistant to Syt2 deletion in immature calyces. This demonstrates a developmental Syt1-Syt2 isoform switch at an identified synapse, a mechanism that could fine-tune the speed, reliability, and plasticity of transmitter release at fast releasing CNS synapses.
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