ArticleNeurobiology of learning and memory2009
Impaired long-term potentiation and enhanced neuronal excitability in the amygdala of Ca(V)1.3 knockout mice.
Article in Neurobiology of learning and memory, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed.
- Role of Cav1.3 Channels in Brain-Heart Interactions: An Unexpected Journey.Biomedicines · 2025Review
- Synaptic potentiation of engram cells is necessary and sufficient for context fear memory.Communications biology · 2025Article
- Voltage-gated calcium channels in genetic epilepsies.Journal of neurochemistry · 2024Review
- A consistent map in the medial entorhinal cortex supports spatial memory.Nature communications · 2024Article
- The human channel gating-modifying A749G CACNA1D (Cav1.3) variant induces a neurodevelopmental syndrome-like phenotype in mice.JCI insight · 2023Article
- A consistent map in the medial entorhinal cortex supports spatial memory.bioRxiv : the preprint server for biology · 2023Article
- Age-related deficits in neuronal physiology and cognitive function are recapitulated in young mice overexpressing the L-type calcium channel, CaAging cell · 2023Article
- Adaptive control of synaptic plasticity integrates micro- and macroscopic network function.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Review
- Anxiety and hippocampal neuronal activity: Relationship and potential mechanisms.Cognitive, affective & behavioral neuroscience · 2022Review
- Snapin Specifically Up-Regulates CaInternational journal of molecular sciences · 2021Article
- Zebrafish Larvae Carrying a Splice Variant Mutation in cacna1d: A New Model for Schizophrenia-Like Behaviours?Molecular neurobiology · 2021Article
- Targeting microglia L-type voltage-dependent calcium channels for the treatment of central nervous system disorders.Journal of neuroscience research · 2021Review
- Brain Pathogenesis and Potential Therapeutic Strategies in Myotonic Dystrophy Type 1.Frontiers in aging neuroscience · 2021Review
- Altered Expression of Ion Channels in White Matter Lesions of Progressive Multiple Sclerosis: What Do We Know About Their Function?Frontiers in cellular neuroscience · 2021Review
- Gene Transcript Alterations in the Spinal Cord, Anterior Cingulate Cortex, and Amygdala in Mice Following Peripheral Nerve Injury.Frontiers in cell and developmental biology · 2021Article
- De novo CACNA1D CaPflugers Archiv : European journal of physiology · 2020Review
- Pre- and post-synaptic roles for DCC in memory consolidation in the adult mouse hippocampus.Molecular brain · 2020Article
- The molecular and cellular mechanisms of depression: a focus on reward circuitry.Molecular psychiatry · 2019Review
- Developmental Aspects of Glucose and Calcium Availability on the Persistence of Memory Function Over the Lifespan.Frontiers in aging neuroscience · 2019Review
- Review
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4 authors.
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Abstract
Previously, we demonstrated that mice in which the gene for the L-type voltage-gated calcium channel Ca(V)1.3 is deleted (Ca(V)1.3 knockout mice) exhibit an impaired ability to consolidate contextually-conditioned fear. Given that this form of Pavlovian fear conditioning is critically dependent on the basolateral complex of the amygdala (BLA), we were interested in the mechanisms by which Ca(V)1.3 contributes to BLA neurophysiology. In the present study, we used in vitro amygdala slices prepared from Ca(V)1.3 knockout mice and wild-type littermates to explore the role of Ca(V)1.3 in long-term potentiation (LTP) and intrinsic neuronal excitability in the BLA. We found that LTP in the lateral nucleus (LA) of the BLA, induced by high-frequency stimulation of the external capsule, was significantly reduced in Ca(V)1.3 knockout mice. Additionally, we found that BLA principal neurons from Ca(V)1.3 knockout mice were hyperexcitable, exhibiting significant increases in firing rates and decreased interspike intervals in response to prolonged somatic depolarization. This aberrant increase in neuronal excitability appears to be at least in part due to a concomitant reduction in the slow component of the post-burst afterhyperpolarization. Together, these results demonstrate altered neuronal function in the BLA of Ca(V)1.3 knockout mice which may account for the impaired ability of these mice to consolidate contextually-conditioned fear.
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