ArticleThe Journal of physiology2014
A novel short-term plasticity of intrinsic excitability in the hippocampal CA1 pyramidal cells.
Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- ATRX function beyond hippocampal CA1 is required for cognitive deficits in mouse models of intellectual disability.PloS one · 2026Article
- Short-term neuronal and synaptic plasticity act in synergy for deviance detection in spiking networks.PLoS computational biology · 2023Article
- A biophysical perspective on the resilience of neuronal excitability across timescales.Nature reviews. Neuroscience · 2023Review
- Neuron populations use variable combinations of short-term feedback mechanisms to stabilize firing rate.PLoS biology · 2023Article
- Article
- Alpha-lipoic acid downregulates TRPV1 receptor via NF-κB and attenuates neuropathic pain in rats with diabetes.CNS neuroscience & therapeutics · 2020Article
- Control of Neuronal Ryanodine Receptor-Mediated Calcium Signaling by Calsenilin.Molecular neurobiology · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in neuronal activity often trigger compensatory mechanisms aimed at regulating network activity homeostatically. Here we have identified and characterized a novel form of compensatory short-term plasticity of membrane excitability, which develops early after the eye-opening period in rats (P16-19 days) but not before that developmental stage (P9-12 days old). Holding the membrane potential of CA1 neurons right below the firing threshold from 15 s to several minutes induced a potentiation of the repolarizing phase of the action potentials that contributed to a decrease in the firing rate of CA1 pyramidal neurons in vitro. Furthermore, the mechanism for inducing this plasticity required the action of intracellular Ca(2+) entering through T-type Ca(2+) channels. This increase in Ca(2+) subsequently activated the Ca(2+) sensor K(+) channel interacting protein 3, which led to the increase of an A-type K(+) current. These results suggest that Ca(2+) modulation of somatic A-current represents a new form of homeostatic regulation that provides CA1 pyramidal neurons with the ability to preserve their firing abilities in response to membrane potential variations on a scale from tens of seconds to several minutes.
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