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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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 |
format | Article |
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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.</description><identifier>ISSN: 0896-6273</identifier><identifier>EISSN: 1097-4199</identifier><identifier>DOI: 10.1016/j.neuron.2018.11.028</identifier><identifier>PMID: 30545599</identifier><language>eng</language><publisher>United States: Elsevier Limited</publisher><subject>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</subject><ispartof>Neuron (Cambridge, Mass.), 2019-01, Vol.101 (2), p.260</ispartof><rights>Copyright © 2018 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Jan 16, 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30545599$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lübbert, Matthias</creatorcontrib><creatorcontrib>Goral, R Oliver</creatorcontrib><creatorcontrib>Keine, Christian</creatorcontrib><creatorcontrib>Thomas, Connon</creatorcontrib><creatorcontrib>Guerrero-Given, Debbie</creatorcontrib><creatorcontrib>Putzke, Travis</creatorcontrib><creatorcontrib>Satterfield, Rachel</creatorcontrib><creatorcontrib>Kamasawa, Naomi</creatorcontrib><creatorcontrib>Young, Jr, Samuel M</creatorcontrib><title>Ca V 2.1 α 1 Subunit Expression Regulates Presynaptic Ca V 2.1 Abundance and Synaptic Strength at a Central Synapse</title><title>Neuron (Cambridge, Mass.)</title><addtitle>Neuron</addtitle><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.</description><subject>Abundance</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Biophysics</subject><subject>Brain Stem - cytology</subject><subject>Cadmium Chloride - pharmacology</subject><subject>Calcium - metabolism</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Calcium channels</subject><subject>Calcium channels (voltage-gated)</subject><subject>Calcium Channels, N-Type - genetics</subject><subject>Calcium Channels, N-Type - metabolism</subject><subject>Developmental stages</subject><subject>Electric Stimulation</subject><subject>Female</subject><subject>Green Fluorescent Proteins - genetics</subject><subject>Green Fluorescent Proteins - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Neurotransmitter Agents - metabolism</subject><subject>Presynaptic Terminals - physiology</subject><subject>Presynaptic Terminals - ultrastructure</subject><subject>Synapses</subject><subject>Synapses - physiology</subject><subject>Synapses - ultrastructure</subject><subject>Synaptic strength</subject><subject>Synaptic transmission</subject><subject>Synaptic Transmission - genetics</subject><issn>0896-6273</issn><issn>1097-4199</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kF9LwzAUxYMobk6_gUjA59bctEmaxzHmHxgoTn0taXM7O7a0pim4j-UX8TNZ2ObTgXvO7x44hFwDi4GBvFvHDnvfuJgzyGKAmPHshIyBaRWloPUpGbNMy0hylYzIRdetGYNUaDgno4SJVAitxyTMDP2gPAb6-0OBLvuid3Wg8-_WY9fVjaOvuOo3JmBHX4bTzpk21CX9x6YDYI0rkRpn6fLoL4NHtwqf1ARq6Axd8Gaztzu8JGeV2XR4ddAJeb-fv80eo8Xzw9Nsuoha4BAiLK1QmTUaLBqNUDJdgdEqM4gKsaqUwLTgiZWVFbosZKagNJhxqeyAVsmE3O7_tr756rEL-brpvRsqcw5SKam0SIbUzSHVF1u0eevrrfG7_DhS8gfDxmuv</recordid><startdate>20190116</startdate><enddate>20190116</enddate><creator>Lübbert, Matthias</creator><creator>Goral, R Oliver</creator><creator>Keine, Christian</creator><creator>Thomas, Connon</creator><creator>Guerrero-Given, Debbie</creator><creator>Putzke, Travis</creator><creator>Satterfield, Rachel</creator><creator>Kamasawa, Naomi</creator><creator>Young, Jr, Samuel M</creator><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20190116</creationdate><title>Ca V 2.1 α 1 Subunit Expression Regulates Presynaptic Ca V 2.1 Abundance and Synaptic Strength at a Central Synapse</title><author>Lübbert, Matthias ; Goral, R Oliver ; Keine, Christian ; Thomas, Connon ; Guerrero-Given, Debbie ; Putzke, Travis ; Satterfield, Rachel ; Kamasawa, Naomi ; Young, Jr, Samuel M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p121t-ecd578da91dea9e1c09f1a978aee7eeff75e4b23d6fd59cb6871cae8267dcd5f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Abundance</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Biophysics</topic><topic>Brain Stem - cytology</topic><topic>Cadmium Chloride - pharmacology</topic><topic>Calcium - metabolism</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Calcium channels</topic><topic>Calcium channels (voltage-gated)</topic><topic>Calcium Channels, N-Type - genetics</topic><topic>Calcium Channels, N-Type - metabolism</topic><topic>Developmental stages</topic><topic>Electric Stimulation</topic><topic>Female</topic><topic>Green Fluorescent Proteins - genetics</topic><topic>Green Fluorescent Proteins - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Neurotransmitter Agents - metabolism</topic><topic>Presynaptic Terminals - physiology</topic><topic>Presynaptic Terminals - ultrastructure</topic><topic>Synapses</topic><topic>Synapses - physiology</topic><topic>Synapses - ultrastructure</topic><topic>Synaptic strength</topic><topic>Synaptic transmission</topic><topic>Synaptic Transmission - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lübbert, Matthias</creatorcontrib><creatorcontrib>Goral, R Oliver</creatorcontrib><creatorcontrib>Keine, Christian</creatorcontrib><creatorcontrib>Thomas, Connon</creatorcontrib><creatorcontrib>Guerrero-Given, Debbie</creatorcontrib><creatorcontrib>Putzke, Travis</creatorcontrib><creatorcontrib>Satterfield, Rachel</creatorcontrib><creatorcontrib>Kamasawa, Naomi</creatorcontrib><creatorcontrib>Young, Jr, Samuel M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Neuron (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lübbert, Matthias</au><au>Goral, R Oliver</au><au>Keine, Christian</au><au>Thomas, Connon</au><au>Guerrero-Given, Debbie</au><au>Putzke, Travis</au><au>Satterfield, Rachel</au><au>Kamasawa, Naomi</au><au>Young, Jr, Samuel M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ca V 2.1 α 1 Subunit Expression Regulates Presynaptic Ca V 2.1 Abundance and Synaptic Strength at a Central Synapse</atitle><jtitle>Neuron (Cambridge, Mass.)</jtitle><addtitle>Neuron</addtitle><date>2019-01-16</date><risdate>2019</risdate><volume>101</volume><issue>2</issue><spage>260</spage><pages>260-</pages><issn>0896-6273</issn><eissn>1097-4199</eissn><abstract>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.</abstract><cop>United States</cop><pub>Elsevier Limited</pub><pmid>30545599</pmid><doi>10.1016/j.neuron.2018.11.028</doi></addata></record> |
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source | MEDLINE; Cell Press Free Archives; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; ScienceDirect Journals (5 years ago - present) |
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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