ArticleThe Journal of physiology2015
Homeostatic regulation of h-conductance controls intrinsic excitability and stabilizes the threshold for synaptic modification in CA1 neurons.
Article in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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31 citing papers in PubMed, 64 citations in OpenAlex.
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- Modular arrangement of synaptic and intrinsic homeostatic plasticity within visual cortical circuits.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- H- and m-channel overexpression promotes seizure-like events by impairing the ability of inhibitory neurons to process correlated inputs.PLoS computational biology · 2025Article
- Modular Arrangement of Synaptic and Intrinsic Homeostatic Plasticity within Visual Cortical Circuits.bioRxiv : the preprint server for biology · 2025Article
- Motor cortical neuronal hyperexcitability associated with α-synuclein aggregation.NPJ Parkinson's disease · 2025Article
- Hyperpolarization-activated cyclic nucleotide-gated channels and epilepsy: genetics, circuits, and treatments.Frontiers in neurology · 2025Review
- Intrinsic plasticity of Purkinje cell serves homeostatic regulation of fear memory.Molecular psychiatry · 2024Article
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- Recurrent network interactions explain tectal response variability and experience-dependent behavior.eLife · 2023Article
- Theta patterns of stimulation induce synaptic and intrinsic potentiation in O-LM interneurons.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- IProgress in neuro-psychopharmacology & biological psychiatry · 2022Article
- Formin Activity and mDia1 Contribute to Maintain Axon Initial Segment Composition and Structure.Molecular neurobiology · 2021Article
- Homeostatic regulation of axonal Kv1.1 channels accounts for both synaptic and intrinsic modifications in the hippocampal CA3 circuit.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Memory destabilization during reconsolidation: a consequence of homeostatic plasticity?Learning & memory (Cold Spring Harbor, N.Y.) · 2021Article
- Homeostatic plasticity and burst activity are mediated by hyperpolarization-activated cation currents and T-type calcium channels in neuronal cultures.Scientific reports · 2021Article
- Circadian rhythm of redox state regulates membrane excitability in hippocampal CA1 neurons.The European journal of neuroscience · 2020Article
- Homeostatic Plasticity in Epilepsy.Frontiers in cellular 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
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3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
key pointsWe determined the contribution of the hyperpolarization-activated cationic (h) current (Ih ) to the homeostatic regulation of CA1 pyramidal cells in vitro using chronic treatments (48 h) that either increase (picrotoxin) or decrease (kynurenate) neuronal activity. The h-conductance was found to be up- or down-regulated following chronic activity enhancement or activity deprivation, respectively. This bidirectional plasticity of Ih was found to subsequently alter both apparent input resistance and intrinsic neuronal excitability. Bidirectional homeostatic plasticity of Ih also determined EPSP waveform and EPSP summation tested at 5-30 Hz. Long-term synaptic modification induced by repetitive stimulation of the Schaffer collaterals was found to be constant across treatments in the presence of Ih but not when Ih was blocked pharmacologically. Thus, bidirectional homeostatic regulation of Ih stabilizes induction of long-term synaptic modification in CA1 pyramidal neurons that depends on EPSP summation. ABSTRACT: The hyperpolarization-activated cationic (h) current is a voltage-shock absorber, highly expressed in the dendrites of CA1 pyramidal neurons. Up-regulation of Ih has been reported following episodes of intense network activity but the effect of activity deprivation on Ih and the functional consequence of homeostatic regulation of Ih remain unclear. We determined here the contribution of Ih to the homeostatic regulation of CA1 pyramidal cell excitability. Intrinsic neuronal excitability was decreased in neurons treated for 2-3 days with the GABAA channel blocker picrotoxin (PiTx) but increased in neurons treated (2-3 days) with the glutamate receptor antagonist kynurenate (Kyn). Membrane capacitance remained unchanged after treatment but the apparent input resistance was reduced for PiTx-treated neurons and enhanced for Kyn-treated neurons. Maximal Ih conductance was up-regulated after chronic hyperactivity but down-regulated following chronic hypoactivity. Up-regulation of Ih in PiTx-treated cultures was found to accelerate EPSP kinetics and reduce temporal summation of EPSPs whereas opposite effects were observed in Kyn-treated cultures, indicating that homeostatic regulation of Ih may control the induction of synaptic modification depending on EPSP summation. In fact, stimulation of the Schaffer collaterals at 3-10 Hz induced differential levels of plasticity in PiTx-treated and Kyn-treated neurons when Ih was blocked pharmacologically but not in control conditions. These data indicate that homeostatic regulation of Ih normalizes the threshold for long-term synaptic modification that depends on EPSP summation. In conclusion, bidirectional homeostatic regulation of Ih not only controls spiking activity but also stabilizes the threshold for long-term potentiation induced in CA1 pyramidal neurons by repetitive stimulation.
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