Ablation of CaV2.1 Voltage-Gated Ca2+ Channels in Mouse Forebrain Generates Multiple Cognitive Impairments
Voltage-gated CaV2.1 (P/Q-type) Ca2+ channels located at the presynaptic membrane are known to control a multitude of Ca2+-dependent cellular processes such as neurotransmitter release and synaptic plasticity. Our knowledge about their contributions to complex cognitive functions, however, is restri...
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description | Voltage-gated CaV2.1 (P/Q-type) Ca2+ channels located at the presynaptic membrane are known to control a multitude of Ca2+-dependent cellular processes such as neurotransmitter release and synaptic plasticity. Our knowledge about their contributions to complex cognitive functions, however, is restricted by the limited adequacy of existing transgenic CaV2.1 mouse models. Global CaV2.1 knock-out mice lacking the α1 subunit Cacna1a gene product exhibit early postnatal lethality which makes them unsuitable to analyse the relevance of CaV2.1 Ca2+ channels for complex behaviour in adult mice. Consequently we established a forebrain specific CaV2.1 knock-out model by crossing mice with a floxed Cacna1a gene with mice expressing Cre-recombinase under the control of the NEX promoter. This novel mouse model enabled us to investigate the contribution of CaV2.1 to complex cognitive functions, particularly learning and memory. Electrophysiological analysis allowed us to test the specificity of our conditional knock-out model and revealed an impaired synaptic transmission at hippocampal glutamatergic synapses. At the behavioural level, the forebrain-specific CaV2.1 knock-out resulted in deficits in spatial learning and reference memory, reduced recognition memory, increased exploratory behaviour and a strong attenuation of circadian rhythmicity. In summary, we present a novel conditional CaV2.1 knock-out model that is most suitable for analysing the in vivo functions of CaV2.1 in the adult murine forebrain. |
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Our knowledge about their contributions to complex cognitive functions, however, is restricted by the limited adequacy of existing transgenic CaV2.1 mouse models. Global CaV2.1 knock-out mice lacking the α1 subunit Cacna1a gene product exhibit early postnatal lethality which makes them unsuitable to analyse the relevance of CaV2.1 Ca2+ channels for complex behaviour in adult mice. Consequently we established a forebrain specific CaV2.1 knock-out model by crossing mice with a floxed Cacna1a gene with mice expressing Cre-recombinase under the control of the NEX promoter. This novel mouse model enabled us to investigate the contribution of CaV2.1 to complex cognitive functions, particularly learning and memory. Electrophysiological analysis allowed us to test the specificity of our conditional knock-out model and revealed an impaired synaptic transmission at hippocampal glutamatergic synapses. At the behavioural level, the forebrain-specific CaV2.1 knock-out resulted in deficits in spatial learning and reference memory, reduced recognition memory, increased exploratory behaviour and a strong attenuation of circadian rhythmicity. In summary, we present a novel conditional CaV2.1 knock-out model that is most suitable for analysing the in vivo functions of CaV2.1 in the adult murine forebrain.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0078598</identifier><identifier>PMID: 24205277</identifier><language>eng</language><publisher>San Francisco: Public Library of Science</publisher><subject>Adequacy ; Alzheimer's disease ; Animal models ; Ataxia ; Behavior ; Brain ; CACNA1A protein ; Calcium channels ; Calcium channels (P/Q-type) ; Calcium channels (Q-type) ; Calcium channels (voltage-gated) ; Channels ; Circadian rhythms ; Cognitive ability ; Dementia ; Experiments ; Exploratory behavior ; Forebrain ; Glutamatergic transmission ; Hippocampus ; Immunoglobulins ; In vivo methods and tests ; Laboratories ; Lethality ; Mathematical models ; Memory ; Mice ; Migraine ; Neurotransmitter release ; Plastic foam ; Recombinase ; Rodents ; Spatial discrimination learning ; Spatial memory ; Synapses ; Synaptic plasticity ; Synaptic transmission ; Transmitters</subject><ispartof>PloS one, 2013-10, Vol.8 (10), p.e78598</ispartof><rights>2013 Mallmann et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Mallmann et al 2013 Mallmann et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3158-507bdebbc7ee22e6f17a432146710ede6e8a3477488008ef7a528c8439d12bf53</citedby><cites>FETCH-LOGICAL-c3158-507bdebbc7ee22e6f17a432146710ede6e8a3477488008ef7a528c8439d12bf53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3814415/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3814415/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2926,23865,27923,27924,53790,53792,79371,79372</link.rule.ids></links><search><contributor>Singh, Brij</contributor><creatorcontrib>Mallmann, Robert Theodor</creatorcontrib><creatorcontrib>Elgueta, Claudio</creatorcontrib><creatorcontrib>Sleman, Faten</creatorcontrib><creatorcontrib>Castonguay, Jan</creatorcontrib><creatorcontrib>Wilmes, Thomas</creatorcontrib><creatorcontrib>van den Maagdenberg, Arn</creatorcontrib><creatorcontrib>Klugbauer, Norbert</creatorcontrib><title>Ablation of CaV2.1 Voltage-Gated Ca2+ Channels in Mouse Forebrain Generates Multiple Cognitive Impairments</title><title>PloS one</title><description>Voltage-gated CaV2.1 (P/Q-type) Ca2+ channels located at the presynaptic membrane are known to control a multitude of Ca2+-dependent cellular processes such as neurotransmitter release and synaptic plasticity. Our knowledge about their contributions to complex cognitive functions, however, is restricted by the limited adequacy of existing transgenic CaV2.1 mouse models. Global CaV2.1 knock-out mice lacking the α1 subunit Cacna1a gene product exhibit early postnatal lethality which makes them unsuitable to analyse the relevance of CaV2.1 Ca2+ channels for complex behaviour in adult mice. Consequently we established a forebrain specific CaV2.1 knock-out model by crossing mice with a floxed Cacna1a gene with mice expressing Cre-recombinase under the control of the NEX promoter. This novel mouse model enabled us to investigate the contribution of CaV2.1 to complex cognitive functions, particularly learning and memory. Electrophysiological analysis allowed us to test the specificity of our conditional knock-out model and revealed an impaired synaptic transmission at hippocampal glutamatergic synapses. At the behavioural level, the forebrain-specific CaV2.1 knock-out resulted in deficits in spatial learning and reference memory, reduced recognition memory, increased exploratory behaviour and a strong attenuation of circadian rhythmicity. In summary, we present a novel conditional CaV2.1 knock-out model that is most suitable for analysing the in vivo functions of CaV2.1 in the adult murine forebrain.</description><subject>Adequacy</subject><subject>Alzheimer's disease</subject><subject>Animal models</subject><subject>Ataxia</subject><subject>Behavior</subject><subject>Brain</subject><subject>CACNA1A protein</subject><subject>Calcium channels</subject><subject>Calcium channels (P/Q-type)</subject><subject>Calcium channels (Q-type)</subject><subject>Calcium channels (voltage-gated)</subject><subject>Channels</subject><subject>Circadian rhythms</subject><subject>Cognitive ability</subject><subject>Dementia</subject><subject>Experiments</subject><subject>Exploratory behavior</subject><subject>Forebrain</subject><subject>Glutamatergic transmission</subject><subject>Hippocampus</subject><subject>Immunoglobulins</subject><subject>In vivo methods and 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of CaV2.1 Voltage-Gated Ca2+ Channels in Mouse Forebrain Generates Multiple Cognitive Impairments</title><author>Mallmann, Robert Theodor ; Elgueta, Claudio ; Sleman, Faten ; Castonguay, Jan ; Wilmes, Thomas ; van den Maagdenberg, Arn ; Klugbauer, Norbert</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3158-507bdebbc7ee22e6f17a432146710ede6e8a3477488008ef7a528c8439d12bf53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adequacy</topic><topic>Alzheimer's disease</topic><topic>Animal models</topic><topic>Ataxia</topic><topic>Behavior</topic><topic>Brain</topic><topic>CACNA1A protein</topic><topic>Calcium channels</topic><topic>Calcium channels (P/Q-type)</topic><topic>Calcium channels (Q-type)</topic><topic>Calcium channels (voltage-gated)</topic><topic>Channels</topic><topic>Circadian rhythms</topic><topic>Cognitive 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one</jtitle><date>2013-10-31</date><risdate>2013</risdate><volume>8</volume><issue>10</issue><spage>e78598</spage><pages>e78598-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Voltage-gated CaV2.1 (P/Q-type) Ca2+ channels located at the presynaptic membrane are known to control a multitude of Ca2+-dependent cellular processes such as neurotransmitter release and synaptic plasticity. Our knowledge about their contributions to complex cognitive functions, however, is restricted by the limited adequacy of existing transgenic CaV2.1 mouse models. Global CaV2.1 knock-out mice lacking the α1 subunit Cacna1a gene product exhibit early postnatal lethality which makes them unsuitable to analyse the relevance of CaV2.1 Ca2+ channels for complex behaviour in adult mice. Consequently we established a forebrain specific CaV2.1 knock-out model by crossing mice with a floxed Cacna1a gene with mice expressing Cre-recombinase under the control of the NEX promoter. This novel mouse model enabled us to investigate the contribution of CaV2.1 to complex cognitive functions, particularly learning and memory. Electrophysiological analysis allowed us to test the specificity of our conditional knock-out model and revealed an impaired synaptic transmission at hippocampal glutamatergic synapses. At the behavioural level, the forebrain-specific CaV2.1 knock-out resulted in deficits in spatial learning and reference memory, reduced recognition memory, increased exploratory behaviour and a strong attenuation of circadian rhythmicity. In summary, we present a novel conditional CaV2.1 knock-out model that is most suitable for analysing the in vivo functions of CaV2.1 in the adult murine forebrain.</abstract><cop>San Francisco</cop><pub>Public Library of Science</pub><pmid>24205277</pmid><doi>10.1371/journal.pone.0078598</doi><oa>free_for_read</oa></addata></record> |
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subjects | Adequacy Alzheimer's disease Animal models Ataxia Behavior Brain CACNA1A protein Calcium channels Calcium channels (P/Q-type) Calcium channels (Q-type) Calcium channels (voltage-gated) Channels Circadian rhythms Cognitive ability Dementia Experiments Exploratory behavior Forebrain Glutamatergic transmission Hippocampus Immunoglobulins In vivo methods and tests Laboratories Lethality Mathematical models Memory Mice Migraine Neurotransmitter release Plastic foam Recombinase Rodents Spatial discrimination learning Spatial memory Synapses Synaptic plasticity Synaptic transmission Transmitters |
title | Ablation of CaV2.1 Voltage-Gated Ca2+ Channels in Mouse Forebrain Generates Multiple Cognitive Impairments |
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