| Literature DB >> 30545599 |
Matthias Lübbert1, R Oliver Goral2, Christian Keine2, Connon Thomas3, Debbie Guerrero-Given3, Travis Putzke1, Rachel Satterfield1, Naomi Kamasawa3, Samuel M Young4.
Abstract
The abundance of presynaptic CaV2 voltage-gated Ca2+ channels (CaV2) at mammalian active zones (AZs) regulates the efficacy of synaptic transmission. It is proposed that presynaptic CaV2 levels are saturated in AZs due to a finite number of slots that set CaV2 subtype abundance and that CaV2.1 cannot compete for CaV2.2 slots. However, at most AZs, CaV2.1 levels are highest and CaV2.2 levels are developmentally reduced. To investigate CaV2.1 saturation states and preference in AZs, we overexpressed the CaV2.1 and CaV2.2 α1 subunits at the calyx of Held at immature and mature developmental stages. We found that AZs prefer CaV2.1 to CaV2.2. Remarkably, CaV2.1 α1 subunit overexpression drove increased CaV2.1 currents and channel numbers and increased synaptic strength at both developmental stages examined. Therefore, we propose that CaV2.1 levels in the AZ are not saturated and that synaptic strength can be modulated by increasing CaV2.1 levels to regulate neuronal circuit output. VIDEO ABSTRACT.Entities:
Keywords: Ca(V)2.1; active zone; calcium channels; calyx of Held; neuronal circuits; release probability; synaptic plasticity; synaptic strength; synaptic transmission; viral vectors
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Year: 2018 PMID: 30545599 PMCID: PMC6413316 DOI: 10.1016/j.neuron.2018.11.028
Source DB: PubMed Journal: Neuron ISSN: 0896-6273 Impact factor: 17.173