ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
KV7/M channels mediate osmotic modulation of intrinsic neuronal excitability.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- KArchiv der Pharmazie · 2026Review
- Persistent Na+ current couples spreading depolarization to seizures in Scn8a gain-of-function mice.Brain : a journal of neurology · 2025Article
- Evaluation of Small-Molecule Candidates as Modulators of M-Type KInternational journal of molecular sciences · 2025Review
- The absence of AQP4/TRPV4 complex substantially reduces acute cytotoxic edema following ischemic injury.Frontiers in cellular neuroscience · 2022Article
- Mannitol decreases neocortical epileptiform activity during early brain development via cotransport of chloride and water.Neurobiology of disease · 2019Article
- Bisoprolol, Known to Be a Selective β₁-Receptor Antagonist, Differentially but Directly Suppresses IInternational journal of molecular sciences · 2019Article
- Article
- Cell Volume Control in Healthy Brain and Neuropathologies.Current topics in membranes · 2018Review
- Turning down the volume: Astrocyte volume change in the generation and termination of epileptic seizures.Neurobiology of disease · 2017Review
- KThe Journal of physiology · 2017Article
- Hippocampal and Cortical Pyramidal Neurons Swell in Parallel with Astrocytes during Acute Hypoosmolar Stress.Frontiers in cellular neuroscience · 2017Article
- The Role of Kv7/M Potassium Channels in Controlling Ectopic Firing in Nociceptors.Frontiers in molecular neuroscience · 2017Article
- Role of small conductance Ca²⁺-activated K⁺ channels in controlling CA1 pyramidal cell excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Electrolyte therapy reduces spike-and-wave discharges in the WAG/Rij rat model of absence epilepsy.Epilepsy & behavior : E&B · 2012Article
- Osmosensitivity through the PIP2 availability: just add water.The Journal of physiology · 2010Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Modest decreases in extracellular osmolarity induce brain hyperexcitability that may culminate in epileptic seizures. At the cellular level, moderate hyposmolarity markedly potentiates the intrinsic neuronal excitability of principal cortical neurons without significantly affecting their volume. The most conspicuous cellular effect of hyposmolarity is converting regular firing neurons to burst-firing mode. This effect is underlain by hyposmotic facilitation of the spike afterdepolarization (ADP), but its ionic mechanism is unknown. Because blockers of K(V)7 (KCNQ) channels underlying neuronal M-type K(+) currents (K(V)7/M channels) also cause spike ADP facilitation and bursting, we hypothesized that lowering osmolarity inhibits these channels. Using current- and voltage-clamp recordings in CA1 pyramidal cells in situ, we have confirmed this hypothesis. Furthermore, we show that hyposmotic inhibition of K(V)7/M channels is mediated by an increase in intracellular Ca(2+) concentration via release from internal stores but not via influx of extracellular Ca(2+). Finally, we show that interfering with internal Ca(2+)-mediated inhibition of K(V)7/M channels entirely protects against hyposmotic ADP facilitation and bursting, indicating the exclusivity of this novel mechanism in producing intrinsic neuronal hyperexcitability in hyposmotic conditions.
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