ReviewFrontiers in systems neuroscience2016
Intrinsic Hippocampal Excitability Changes of Opposite Signs and Different Origins in CA1 and CA3 Pyramidal Neurons Underlie Aging-Related Cognitive Deficits.
Review in Frontiers in systems neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Pooled it
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- FCGR2B knockdown alleviates diabetes-induced cognitive dysfunction by altering neuronal excitability.Molecular medicine (Cambridge, Mass.) · 2025Article
- Age-related synaptic signatures of brain and cognitive reserve in the rat hippocampus and parahippocampal regions.Neurobiology of aging · 2025Article
- Somatostatin: Linking Cognition and Alzheimer Disease to Therapeutic Targeting.Pharmacological reviews · 2024Review
- Type-2 Diabetes Alters Hippocampal Neural Oscillations and Disrupts Synchrony between the Hippocampus and Cortex.Aging and disease · 2024Article
- Overexpression of KCNN4 channels in principal neurons produces an anti-seizure effect without reducing their coding ability.Gene therapy · 2024Article
- Genetic Ablation of Dentate Hilar Somatostatin-Positive GABAergic Interneurons is Sufficient to Induce Cognitive Impairment.Molecular neurobiology · 2024Article
- Article
- Liver-expressed antimicrobial peptide 2 elevation contributes to age-associated cognitive decline.JCI insight · 2023Article
- The lncRNAbioRxiv : the preprint server for biology · 2023Article
- Selective inhibition of somatostatin-positive dentate hilar interneurons induces age-related cellular changes and cognitive dysfunction.PNAS nexus · 2023Article
- Article
- The times they are a-changin': a proposal on how brain flexibility goes beyond the obvious to include the concepts of "upward" and "downward" to neuroplasticity.Molecular psychiatry · 2023Review
- Sex Differences in Cognition Across Aging.Current topics in behavioral neurosciences · 2023Review
- Sensitivity of the S1 neuronal calcium network to insulin and Bay-K 8644 in vivo: Relationship to gait, motivation, and aging processes.Aging cell · 2022Article
- Dysregulation ofLearning & memory (Cold Spring Harbor, N.Y.) · 2022Article
- A Neuroscience Primer for Integrating Geroscience With the Neurobiology of Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022Article
- Altered membrane properties but unchanged intrinsic excitability and spontaneous postsynaptic currents in an aged APPFrontiers in cellular neuroscience · 2022Article
- Increased hippocampal excitability in miR-324-null mice.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Aging-related cognitive deficits have been attributed to dysfunction of neurons due to failures at synaptic or intrinsic loci, or both. Given the importance of the hippocampus for successful encoding of memory and that the main output of the hippocampus is via the CA1 pyramidal neurons, much of the research has been focused on identifying the aging-related changes of these CA1 pyramidal neurons. We and others have discovered that the postburst afterhyperpolarization (AHP) following a train of action potentials is greatly enlarged in CA1 pyramidal neurons of aged animals. This enlarged postburst AHP is a significant factor in reducing the intrinsic excitability of these neurons, and thus limiting their activity in the neural network during learning. Based on these data, it has largely been thought that aging-related cognitive deficits are attributable to reduced activity of pyramidal neurons. However, recent in vivo and ex vivo studies provide compelling evidence that aging-related deficits could also be due to a converse change in CA3 pyramidal neurons, which show increased activity with aging. In this review, we will incorporate these recent findings and posit that an interdependent dynamic dysfunctional change occurs within the hippocampal network, largely due to altered intrinsic excitability in CA1 and CA3 hippocampal pyramidal neurons, which ultimately leads to the aging-related cognitive deficits.
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Registered trials
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.