ArticleScientific reports2022
A glibenclamide-sensitive TRPM4-mediated component of CA1 excitatory postsynaptic potentials appears in experimental autoimmune encephalomyelitis.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- SUR1-TRPM4 is expressed in human epilepsy and promotes neuron hyperactivity and seizures in rodents.Brain : a journal of neurology · 2026Article
- TRP Channels from Sensory Coding to Physiology.Metabolites · 2025Review
- Multidimensional pan cancer analysis of the sodium induced cell death gene TRPM4.Scientific reports · 2025Article
- The nonsteroidal anti-inflammatory drug meclofenamate mitigates kainic acid-induced seizures via TRPM4 inhibition.Brain communications · 2025Article
- Identification and development of TRPM4 antagonists to counteract neuronal excitotoxicity.iScience · 2024Article
- TRPM4 regulates hilar mossy cell loss in temporal lobe epilepsy.BMC biology · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
The transient receptor potential melastatin 4 (TRPM4) channel contributes to disease severity in the murine experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis and to neuronal cell death in models of excitotoxicity and traumatic brain injury. As TRPM4 is activated by intracellular calcium and conducts monovalent cations, we hypothesized that TRPM4 may contribute to and boost excitatory synaptic transmission in CA1 pyramidal neurons of the hippocampus. Using single-spine calcium imaging and electrophysiology, we found no effect of the TRPM4 antagonists 9-phenanthrol and glibenclamide on synaptic transmission in hippocampal slices from healthy mice. In contrast, glibenclamide but not 9-phenanthrol reduced excitatory synaptic potentials in slices from EAE mice, an effect that was absent in slices from EAE mice lacking TRPM4. We conclude that TRPM4 plays little role in basal hippocampal synaptic transmission, but a glibenclamide-sensitive TRPM4-mediated contribution to excitatory postsynaptic responses is upregulated at the acute phase of EAE.
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