ArticleeNeuro
The Neuropsychiatric Disease-Associated Gene cacna1c Mediates Survival of Young Hippocampal Neurons.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed.
- Article
- P7C3-A20 prevents whole brain radiotherapy-induced chronic hippocampal redox imbalance and neuropsychiatric impairment in mice.Redox biology · 2026Article
- Pharmacologic reversal of advanced Alzheimer's disease in mice and identification of potential therapeutic nodes in human brain.Cell reports. Medicine · 2026Article
- Astrocytic abnormalities in brain-specificChannels (Austin, Tex.) · 2025Article
- Inhibiting 15-PGDH blocks blood-brain barrier deterioration and protects mice from Alzheimer's disease and traumatic brain injury.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- TAAR9 knockout increases hippocampal serotonin and alters grooming behavior in rats.Frontiers in pharmacology · 2025Article
- Cacna1c deficiency in forebrain glutamatergic neurons alters behavior and hippocampal plasticity in female mice.Translational psychiatry · 2024Article
- Acutely blocking excessive mitochondrial fission prevents chronic neurodegeneration after traumatic brain injury.Cell reports. Medicine · 2024Article
- L-type calcium channels and neuropsychiatric diseases: Insights into genetic risk variant-associated genomic regulation and impact on brain development.Channels (Austin, Tex.) · 2023Review
- Application of P7C3 Compounds to Investigating and Treating Acute and Chronic Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- BDNF Levels According to Variations in the CACNA1C Gene: Sex-Based Disparity.Cellular and molecular neurobiology · 2023Article
- Downregulation of neurodevelopmental gene expression in iPSC-derived cerebral organoids upon infection by human cytomegalovirus.iScience · 2022Article
- Maternal P7C3-A20 Treatment Protects Offspring from Neuropsychiatric Sequelae of Prenatal Stress.Antioxidants & redox signaling · 2021Article
- Dual-process brain mitochondria isolation preserves function and clarifies protein composition.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Targeting microglia L-type voltage-dependent calcium channels for the treatment of central nervous system disorders.Journal of neuroscience research · 2021Review
- Methylome Patterns of Cattle Adaptation to Heat Stress.Frontiers in genetics · 2021Article
- Loss of Cav1.2 channels impairs hippocampal theta burst stimulation-induced long-term potentiation.Channels (Austin, Tex.) · 2020Article
- P7C3-A20 treatment one year after TBI in mice repairs the blood-brain barrier, arrests chronic neurodegeneration, and restores cognition.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Conversion of Neural Stem Cells into Functional Neuron-Like Cells by MicroRNA-218: Differential Expression of Functionality Genes.Neurotoxicity research · 2020Article
- The role of L-type calcium channels in neuronal excitability and aging.Neurobiology of learning and memory · 2020Review
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Authors and funding
13 authors.
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Abstract
Genetic variations in CACNA1C, which encodes the Cav1.2 subunit of L-type calcium channels (LTCCs), are associated with multiple forms of neuropsychiatric disease that manifest high anxiety in patients. In parallel, mice harboring forebrain-specific conditional knockout of cacna1c (forebrain-Cav1.2 cKO) display unusually high anxiety-like behavior. LTCCs in general, including the Cav1.3 subunit, have been shown to mediate differentiation of neural precursor cells (NPCs). However, it has not previously been determined whether Cav1.2 affects postnatal hippocampal neurogenesis in vivo. Here, we show that forebrain-Cav1.2 cKO mice exhibit enhanced cell death of young hippocampal neurons, with no change in NPC proliferation, hippocampal size, dentate gyrus thickness, or corticosterone levels compared with wild-type littermates. These mice also exhibit deficits in brain levels of brain-derived neurotrophic factor (BDNF), and Cre recombinase-mediated knockdown of adult hippocampal Cav1.2 recapitulates the deficit in young hippocampal neurons survival. Treatment of forebrain-Cav1.2 cKO mice with the neuroprotective agent P7C3-A20 restored the net magnitude of postnatal hippocampal neurogenesis to wild-type levels without ameliorating their deficit in BDNF expression. The role of Cav1.2 in young hippocampal neurons survival may provide new approaches for understanding and treating neuropsychiatric disease associated with aberrations in CACNA1C. Visual Abstract.
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