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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Veröffentlicht in:PloS one 2013-10, Vol.8 (10), p.e78598
Hauptverfasser: Mallmann, Robert Theodor, Elgueta, Claudio, Sleman, Faten, Castonguay, Jan, Wilmes, Thomas, van den Maagdenberg, Arn, Klugbauer, Norbert
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container_start_page e78598
container_title PloS one
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creator Mallmann, Robert Theodor
Elgueta, Claudio
Sleman, Faten
Castonguay, Jan
Wilmes, Thomas
van den Maagdenberg, Arn
Klugbauer, Norbert
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. 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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.</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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