ArticleJournal of neurophysiology2010
Redox sensitive calcium stores underlie enhanced after hyperpolarization of aged neurons: role for ryanodine receptor mediated calcium signaling.
Article in Journal of neurophysiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 85 citations in OpenAlex.
- Calmodulin controls spatial and temporal specificity of calcium-induced calcium release.PLoS computational biology · 2026Article
- Hydro-Alcoholic Extract of Cynodon dactylon Ameliorates Malathion-Induced Neurocognitive Behavior and Neurotoxicity.Neuromolecular medicine · 2025Article
- Sex, senescence, senolytics, and cognition.Frontiers in aging neuroscience · 2025Review
- Subcellular localization of hippocampal ryanodine receptor 2 and its role in neuronal excitability and memory.Communications biology · 2022Article
- Article
- Limiting RyR2 Open Time Prevents Alzheimer's Disease-Related Neuronal Hyperactivity and Memory Loss but Not β-Amyloid Accumulation.Cell reports · 2020Article
- The role of L-type calcium channels in neuronal excitability and aging.Neurobiology of learning and memory · 2020Review
- Redox Post-translational Modifications of Protein Thiols in Brain Aging and Neurodegenerative Conditions-Focus on S-Nitrosation.Frontiers in aging neuroscience · 2020Review
- Memory and Learning Deficits Are Associated With CaFrontiers in aging neuroscience · 2020Article
- Regulation of intrinsic excitability: Roles for learning and memory, aging and Alzheimer's disease, and genetic diversity.Neurobiology of learning and memory · 2019Review
- Senescent neurophysiology: CaNeurobiology of learning and memory · 2019Review
- Expression of a Constitutively Active Human Insulin Receptor in Hippocampal Neurons Does Not Alter VGCC Currents.Neurochemical research · 2019Article
- Age and Ketogenic Diet Have Dissociable Effects on Synapse-Related Gene Expression Between Hippocampal Subregions.Frontiers in aging neuroscience · 2019Article
- Alteration in NMDA Receptor Mediated Glutamatergic Neurotransmission in the Hippocampus During Senescence.Neurochemical research · 2019Review
- Redox Signaling in Neurotransmission and Cognition During Aging.Antioxidants & redox signaling · 2018Review
- Neuronal Ryanodine Receptors in Development and Aging.Molecular neurobiology · 2018Review
- Ryanodine Receptor-Mediated Calcium Release Has a Key Role in Hippocampal LTD Induction.Frontiers in cellular neuroscience · 2018Article
- Specific ion channels contribute to key elements of pathology during secondary degeneration following neurotrauma.BMC neuroscience · 2017Article
- Aging Impairs Hippocampal- Dependent Recognition Memory and LTP and Prevents the Associated RyR Up-regulation.Frontiers in aging neuroscience · 2017Article
- CA1 pyramidal cells have diverse biophysical properties, affected by development, experience, and aging.PeerJ · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A decrease in the excitability of CA1 pyramidal neurons contributes to the age related decrease in hippocampal function and memory decline. Decreased neuronal excitability in aged neurons can be observed as an increase in the Ca(2+)- activated K(+)- mediated post burst afterhyperpolarization (AHP). In this study, we demonstrate that the slow component of AHP (sAHP) in aged CA1 neurons (aged-sAHP) is decreased ∼50% by application of the reducing agent dithiothreitol (DTT). The DTT-mediated decrease in the sAHP was age specific, such that it was observed in CA1 pyramidal neurons of aged (20-25 mo), but not young (6-9 mo) F344 rats. The effect of DTT on the aged-sAHP was blocked following depletion of intracellular Ca(2+) stores (ICS) by thapsigargin or blockade of ryanodine receptors (RyRs) by ryanodine, suggesting that the age-related increase in the sAHP was due to release of Ca(2+) from ICS through redox sensitive RyRs. The DTT-mediated decrease in the aged-sAHP was not blocked by inhibition of L-type voltage gated Ca(2+) channels (L-type VGCC), inhibition of Ser/Thr kinases, or inhibition of the large conductance BK potassium channels. The results add support to the idea that a shift in the intracellular redox state contributes to Ca(2+) dysregulation during aging.
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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.