ArticleThe Journal of physiology2017
K
Article in The Journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 33 citations in OpenAlex.
- KArchiv der Pharmazie · 2026Review
- Argon improves microglia-mediated hippocampal neuronal hyperexcitability to alleviate anxiety-like behaviors in mice.Journal of molecular cell biology · 2025Article
- Mechanistic correlation of potassium channel sensing and nitric oxide activity in neuroinflammation.Molecular biology reports · 2025Review
- Inflammation differentially controls transport of depolarizing Nav versus hyperpolarizing Kv channels to drive rat nociceptor activity.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Antagonism of the Muscarinic Acetylcholine Type 1 Receptor Enhances Mitochondrial Membrane Potential and Expression of Respiratory Chain Components via AMPK in Human Neuroblastoma SH-SY5Y Cells and Primary Neurons.Molecular neurobiology · 2022Article
- Immune-Triggered Forms of Plasticity Across Brain Regions.Frontiers in cellular neuroscience · 2022Review
- Microglia-triggered hypoexcitability plasticity of pyramidal neurons in the rat medial prefrontal cortex.Current research in neurobiology · 2022Article
- A Proinflammatory Stimulus Disrupts Hippocampal Plasticity and Learning via Microglial Activation and 25-Hydroxycholesterol.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Kcnq2/Kv7.2 controls the threshold and bi-hemispheric symmetry of cortical spreading depolarization.Brain : a journal of neurology · 2021Article
- A Destruction Model of the Vascular and Lymphatic Systems in the Emergence of Psychiatric Symptoms.Biology · 2021Review
- Altered Expression of Ion Channels in White Matter Lesions of Progressive Multiple Sclerosis: What Do We Know About Their Function?Frontiers in cellular neuroscience · 2021Review
- Prevention of brain damage after traumatic brain injury by pharmacological enhancement of KCNQ (Kv7, "M-type") KJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Megalencephalic Leukoencephalopathy with Subcortical Cysts Protein-1 (MLC1) Counteracts Astrocyte Activation in Response to Inflammatory Signals.Molecular neurobiology · 2019Article
- Early Life Inflammation Increases CA1 Pyramidal Neuron Excitability in a Sex and Age Dependent Manner through a Chloride Homeostasis Disruption.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Article
- Reversal of a Treatment-Resistant, Depression-Related Brain State with the Kv7 Channel Opener Retigabine.Neuroscience · 2019Article
- Alleviation of Microglial Activation Induced by p38 MAPK/MK2/PGEScientific reports · 2017Article
- A mechanistic link between glia and neuronal excitability in acute neuroinflammation.The Journal of physiology · 2017Article
- The Role of Kv7/M Potassium Channels in Controlling Ectopic Firing in Nociceptors.Frontiers in molecular neuroscience · 2017Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
key pointsNeuroinflammation associated with CNS insults leads to neuronal hyperexcitability, which may culminate in epileptiform discharges. Application of the endotoxin lipopolysaccharide (LPS) to brain tissue initiates a neuroinflammatory cascade, providing an experimental model to study the mechanisms of neuroinflammatory neuronal hyperexcitability. Here we show that LPS application to hippocampal slices markedly enhances the excitability of CA1 pyramidal cells by inhibiting a specific potassium current, the M-current, generated by K ABSTRACT: Acute brain insults and many chronic brain diseases manifest an innate inflammatory response. The hallmark of this response is glia activation, which promotes repair of damaged tissue, but also induces structural and functional changes that may lead to an increase in neuronal excitability. We have investigated the mechanisms involved in the modulation of neuronal activity by acute inflammation. Initiating inflammatory responses in hippocampal tissue rapidly led to neuronal depolarization and repetitive firing even in the absence of active synaptic transmission. This action was mediated by a complex metabotropic purinergic and glutamatergic glia-to-neuron signalling cascade, leading to the blockade of neuronal K
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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.