ArticleFrontiers in aging neuroscience2010
Learning and aging related changes in intrinsic neuronal excitability.
Article in Frontiers in aging neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed.
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- Potassium homeostasis during disease progression of Alzheimer's disease.The Journal of physiology · 2025Article
- Associative Learning-Induced Synaptic Potentiation at the Two Major Hippocampal CA1 Inputs for Cued Memory Acquisition.Neuroscience bulletin · 2025Article
- Loose-patch clamp analysis applied to voltage-gated ionic currents following pharmacological ryanodine receptor modulation in murine hippocampal cornu ammonis-1 pyramidal neurons.Frontiers in physiology · 2024Article
- A biophysical minimal model to investigate age-related changes in CA1 pyramidal cell electrical activity.PloS one · 2024Article
- Neuroprotective Effects of Ferrostatin and Necrostatin Against Entorhinal Amyloidopathy-Induced Electrophysiological Alterations Mediated by voltage-gated CaNeurochemical research · 2024Article
- Progressive Excitability Changes in the Medial Entorhinal Cortex in the 3xTg Mouse Model of Alzheimer's Disease Pathology.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Progressive excitability changes in the medial entorhinal cortex in the 3xTg mouse model of Alzheimer's disease pathology.bioRxiv : the preprint server for biology · 2023Article
- Antihypertensive drugs and brain function: mechanisms underlying therapeutically beneficial and harmful neuropsychiatric effects.Cardiovascular research · 2023Review
- Age-related deficits in neuronal physiology and cognitive function are recapitulated in young mice overexpressing the L-type calcium channel, CaAging cell · 2023Article
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- Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation.Frontiers in human neuroscience · 2023Article
- Modulation of L-type calcium channels in Alzheimer's disease: A potential therapeutic target.Computational and structural biotechnology journal · 2023Review
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- Mitochondrial CaCommunications biology · 2022Article
- Ghrelin infusion into the basolateral amygdala suppresses CTA memory formation in rats via the PI3K/Akt/mTOR and PLC/PKC signaling pathways.Acta pharmacologica Sinica · 2022Article
- CCR5 closes the temporal window for memory linking.Nature · 2022Article
- Accumulation of C-terminal cleaved tau is distinctly associated with cognitive deficits, synaptic plasticity impairment, and neurodegeneration in aged mice.GeroScience · 2022Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors.
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Abstract
A goal of many laboratories that study aging is to find a key cellular change(s) that can be manipulated and restored to a young-like state, and thus, reverse the age-related cognitive deficits. We have chosen to focus our efforts on the alteration of intrinsic excitability (as reflected by the postburst afterhyperpolarization, AHP) during the learning process in hippocampal pyramidal neurons. We have consistently found that the postburst AHP is significantly reduced in hippocampal pyramidal neurons from young adults that have successfully learned a hippocampus-dependent task. In the context of aging, the baseline intrinsic excitability of hippocampal neurons is decreased and therefore cognitive learning is impaired. In aging animals that are able to learn, neuron changes in excitability similar to those seen in young neurons during learning occur. Our challenge, then, is to understand how and why excitability changes occur in neurons from aging brains and cause age-associated learning impairments. After understanding the changes, we should be able to formulate strategies for reversing them, thus making old neurons function more as they did when they were young. Such a reversal should rescue the age-related cognitive deficits.
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