| First Author | Kochubey O | Year | 2016 |
| Journal | Neuron | Volume | 90 |
| Issue | 5 | Pages | 984-99 |
| PubMed ID | 27210552 | Mgi Jnum | J:239642 |
| Mgi Id | MGI:5829339 | Doi | 10.1016/j.neuron.2016.04.038 |
| Citation | Kochubey O, et al. (2016) A Synaptotagmin Isoform Switch during the Development of an Identified CNS Synapse. Neuron 90(5):984-99 |
| abstractText | 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. |
