Ca V 2.1 α 1 Subunit Expression Regulates Presynaptic Ca V 2.1 Abundance and Synaptic Strength at a Central Synapse

The abundance of presynaptic Ca 2 voltage-gated Ca channels (Ca 2) at mammalian active zones (AZs) regulates the efficacy of synaptic transmission. It is proposed that presynaptic Ca 2 levels are saturated in AZs due to a finite number of slots that set Ca 2 subtype abundance and that Ca 2.1 cannot...

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Veröffentlicht in:Neuron (Cambridge, Mass.) Mass.), 2019-01, Vol.101 (2), p.260
Hauptverfasser: Lübbert, Matthias, Goral, R Oliver, Keine, Christian, Thomas, Connon, Guerrero-Given, Debbie, Putzke, Travis, Satterfield, Rachel, Kamasawa, Naomi, Young, Jr, Samuel M
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container_issue 2
container_start_page 260
container_title Neuron (Cambridge, Mass.)
container_volume 101
creator Lübbert, Matthias
Goral, R Oliver
Keine, Christian
Thomas, Connon
Guerrero-Given, Debbie
Putzke, Travis
Satterfield, Rachel
Kamasawa, Naomi
Young, Jr, Samuel M
description The abundance of presynaptic Ca 2 voltage-gated Ca channels (Ca 2) at mammalian active zones (AZs) regulates the efficacy of synaptic transmission. It is proposed that presynaptic Ca 2 levels are saturated in AZs due to a finite number of slots that set Ca 2 subtype abundance and that Ca 2.1 cannot compete for Ca 2.2 slots. However, at most AZs, Ca 2.1 levels are highest and Ca 2.2 levels are developmentally reduced. To investigate Ca 2.1 saturation states and preference in AZs, we overexpressed the Ca 2.1 and Ca 2.2 α subunits at the calyx of Held at immature and mature developmental stages. We found that AZs prefer Ca 2.1 to Ca 2.2. Remarkably, Ca 2.1 α subunit overexpression drove increased Ca 2.1 currents and channel numbers and increased synaptic strength at both developmental stages examined. Therefore, we propose that Ca 2.1 levels in the AZ are not saturated and that synaptic strength can be modulated by increasing Ca 2.1 levels to regulate neuronal circuit output. VIDEO ABSTRACT.
doi_str_mv 10.1016/j.neuron.2018.11.028
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It is proposed that presynaptic Ca 2 levels are saturated in AZs due to a finite number of slots that set Ca 2 subtype abundance and that Ca 2.1 cannot compete for Ca 2.2 slots. However, at most AZs, Ca 2.1 levels are highest and Ca 2.2 levels are developmentally reduced. To investigate Ca 2.1 saturation states and preference in AZs, we overexpressed the Ca 2.1 and Ca 2.2 α subunits at the calyx of Held at immature and mature developmental stages. We found that AZs prefer Ca 2.1 to Ca 2.2. Remarkably, Ca 2.1 α subunit overexpression drove increased Ca 2.1 currents and channel numbers and increased synaptic strength at both developmental stages examined. Therefore, we propose that Ca 2.1 levels in the AZ are not saturated and that synaptic strength can be modulated by increasing Ca 2.1 levels to regulate neuronal circuit output. 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subjects Abundance
Animals
Animals, Newborn
Biophysics
Brain Stem - cytology
Cadmium Chloride - pharmacology
Calcium - metabolism
Calcium Channel Blockers - pharmacology
Calcium channels
Calcium channels (voltage-gated)
Calcium Channels, N-Type - genetics
Calcium Channels, N-Type - metabolism
Developmental stages
Electric Stimulation
Female
Green Fluorescent Proteins - genetics
Green Fluorescent Proteins - metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Neurotransmitter Agents - metabolism
Presynaptic Terminals - physiology
Presynaptic Terminals - ultrastructure
Synapses
Synapses - physiology
Synapses - ultrastructure
Synaptic strength
Synaptic transmission
Synaptic Transmission - genetics
title Ca V 2.1 α 1 Subunit Expression Regulates Presynaptic Ca V 2.1 Abundance and Synaptic Strength at a Central Synapse
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