ArticleBehavioural brain research2017
A novel mouse model of the aged brain: Over-expression of the L-type voltage-gated calcium channel Ca
Article in Behavioural brain research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- The Impact of Overexpression of the Mouse Ortholog ofBiological psychiatry global open science · 2025Article
- Article
- Age-related deficits in neuronal physiology and cognitive function are recapitulated in young mice overexpressing the L-type calcium channel, CaAging cell · 2023Article
- Deletion of the voltage-gated calcium channel, CaGenes, brain, and behavior · 2022Article
- Deficits across multiple behavioral domains align with susceptibility to stress in 129S1/SvImJ mice.Neurobiology of stress · 2020Article
- The role of L-type calcium channels in neuronal excitability and aging.Neurobiology of learning and memory · 2020Review
- Environmental variables that ameliorate extinction learning deficits in the 129S1/SvlmJ mouse strain.Genes, brain, and behavior · 2019Article
- DNA methylation in the human frontal cortex reveals a putative mechanism for age-by-disease interactions.Translational psychiatry · 2019Article
- Weakened Intracellular ZnMolecular neurobiology · 2018Article
- Membrane ion Channels and Receptors in Animal lifespan Modulation.Journal of cellular physiology · 2017Review
- Article
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Authors and funding
6 authors.
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Abstract
The aged population is growing rapidly, which has sparked tremendous interest in elucidating mechanisms of aging in both the body and the brain. Animal models have become an indispensable tool in biomedical science, but because of the cost and extended timeframe associated with aging animals to appropriate time points, studies that rely on using aged animals are often not feasible. Somewhat surprisingly, there are relatively few animal models that have been specifically engineered to mimic physiological changes known to occur during "normal" aging. Developing transgenic animal models that faithfully mimic key aspects of aging would likely be of great utility in studying both age-related deficits in the absence of overt pathology as well as an adjunct for transgenic models of diseases where aging is a primary risk factor. In particular, there are several alterations in the aged brain that are amenable to being modeled genetically. We have focused on one key aspect that has been repeatedly demonstrated in aged animals - an increase in the L-type voltage-gated calcium channel Ca
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