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- W2408220373 abstract "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 Ca(2+)-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." @default.
- W2408220373 created "2016-06-24" @default.
- W2408220373 creator A5028259248 @default.
- W2408220373 creator A5041607130 @default.
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- W2408220373 date "2016-06-01" @default.
- W2408220373 modified "2023-10-07" @default.
- W2408220373 title "A Synaptotagmin Isoform Switch during the Development of an Identified CNS Synapse" @default.
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- W2408220373 doi "https://doi.org/10.1016/j.neuron.2016.04.038" @default.
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