ArticlePloS one2013
Ablation of Ca(V)2.1 voltage-gated Ca²⁺ channels in mouse forebrain generates multiple cognitive impairments.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Calcium channelopathies and intellectual disability: a systematic review.Orphanet journal of rare diseases · 2021Pooled it
- Neural Correlates of Intellectual Dysfunction in Episodic Ataxia Type 2.Journal of clinical neurology (Seoul, Korea) · 2026Article
- Spatial genomics of AAV vectors reveals mechanism of transcriptional crosstalk that enables targeted delivery of large genetic cargo.Nature biotechnology · 2026Article
- CACNA1A haploinsufficiency leads to reduced synaptic function and increased intrinsic excitability.Brain : a journal of neurology · 2025Article
- Nanoarchitecture of CaBrain pathology (Zurich, Switzerland) · 2025Article
- Genome-wide DNA methylation analysis of hippocampal tissue in a murine model of attention deficit-hyperactivity disorder.PloS one · 2025Article
- Intellectual Disability in Episodic Ataxia Type 2: Beyond Paroxysmal Vertigo and Ataxia.Journal of clinical neurology (Seoul, Korea) · 2024Article
- Intrafamilial neurological phenotypic variability due to either biallelic or monoallelic pathogenic variants inFrontiers in neurology · 2024Article
- The genotype-phenotype correlations of theFrontiers in molecular neuroscience · 2023Article
- Alterations of presynaptic proteins in autism spectrum disorder.Frontiers in molecular neuroscience · 2022Review
- Prioritizing Suggestive Candidate Genes in Migraine: An Opinion.Frontiers in neurology · 2022Article
- Reversing frontal disinhibition rescues behavioural deficits in models of CACNA1A-associated neurodevelopment disorders.Molecular psychiatry · 2021Article
- Elevating the Levels of Calcium Ions Exacerbate Alzheimer's Disease via Inducing the Production and Aggregation of β-Amyloid Protein and Phosphorylated Tau.International journal of molecular sciences · 2021Review
- Enhanced hippocampal type II theta activity AND altered theta architecture in mice lacking the CaScientific reports · 2021Article
- From Genotype to Phenotype: Expanding the Clinical Spectrum ofFrontiers in neurology · 2021Review
- Genetic Inactivation of Two-Pore Channel 1 Impairs Spatial Learning and Memory.Behavior genetics · 2020Article
- Auxiliary α2δ1 and α2δ3 Subunits of Calcium Channels Drive Excitatory and Inhibitory Neuronal Network Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Poor mother-offspring relationships in rats with Cacna1a mutation.Experimental animals · 2020Article
- Genetic Associations between Voltage-Gated Calcium Channels and Psychiatric Disorders.International journal of molecular sciences · 2019Review
- CaNeuron · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated Ca(V)2.1 (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 Ca(V)2.1 mouse models. Global Ca(V)2.1 knock-out mice lacking the α1 subunit Cacna1a gene product exhibit early postnatal lethality which makes them unsuitable to analyse the relevance of Ca(V)2.1 Ca²⁺ channels for complex behaviour in adult mice. Consequently we established a forebrain specific Ca(V)2.1 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 Ca(V)2.1 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 Ca(V)2.1 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 Ca(V)2.1 knock-out model that is most suitable for analysing the in vivo functions of Ca(V)2.1 in the adult murine forebrain.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.