ArticleThe Journal of physiology2018
Functional up-regulation of the M-current by retigabine contrasts hyperexcitability and excitotoxicity on rat hypoglossal motoneurons.
Article in The Journal of physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- The effect of M-current activation on controller gain and obstructive sleep apnoea severity: a randomised controlled trial using flupirtine.The Journal of physiology · 2025Trial
- Novel Dual Mechanism GRT-X Agonist Acting on Kv7 Potassium Channel/Translocator Protein Receptor Prevents Motoneuron Degeneration Following Exposure to Mouse and Human Amyotrophic Lateral Sclerosis/Frontotemporal Dementia Astrocyte-Conditioned Media.ACS chemical neuroscience · 2025Article
- Cholinergic modulation of upper airway control: maturational changes and mechanisms at cellular and synaptic levels.Journal of neurophysiology · 2025Review
- ICA-27243 improves neuromuscular function and preserves motoneurons in the transgenic SOD1Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Phox2b-expressing neurons contribute to breathing problems in Kcnq2 loss- and gain-of-function encephalopathy models.Nature communications · 2023Article
- Genetic Knockout of TRPM2 Increases Neuronal Excitability of Hippocampal Neurons by Inhibiting Kv7 Channel in Epilepsy.Molecular neurobiology · 2022Article
- Therapeutic Targets in Amyotrophic Lateral Sclerosis: Focus on Ion Channels and Skeletal Muscle.Cells · 2022Review
- Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Lysosomes as a therapeutic target.Nature reviews. Drug discovery · 2019Review
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
key pointsExcessive neuronal excitability characterizes several neuropathological conditions, including neurodegenerative diseases such as amyotrophic lateral sclerosis. Hypoglossal motoneurons (HMs), which control tongue muscles, are extremely vulnerable to this disease and undergo damage and death when exposed to an excessive glutamate extracellular concentration that causes excitotoxicity. Our laboratory devised an in vitro model of excitotoxicity obtained by pharmacological blockade of glutamate transporters. In this paradigm, HMs display hyperexcitability, collective bursting and eventually cell death. The results of the present study show that pharmacological up-regulation of a K ABSTRACT: Neuronal hyperexcitability is a symptom characterizing several neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS). In the ALS bulbar form, hypoglossal motoneurons (HMs) are an early target for neurodegeneration because of their high vulnerability to metabolic insults. In recent years, our laboratory has developed an in vitro model of a brainstem slice comprising the hypoglossal nucleus in which HM neurodegeneration is achieved by blocking glutamate clearance with dl-threo-β-benzyloxyaspartate (TBOA), thus leading to delayed excitotoxicity. During this process, HMs display a set of hallmarks such as hyperexcitability (and network bursting), reactive oxygen species (ROS) generation and, finally, cell death. The present study aimed to investigate whether blocking early hyperexcitability and bursting with the anti-convulsant drug retigabine was sufficient to achieve neuroprotection against excitotoxicity. Retigabine is a selective positive allosteric modulator of the M-current (I
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