ArticlePflugers Archiv : European journal of physiology2016
TRPM4-dependent post-synaptic depolarization is essential for the induction of NMDA receptor-dependent LTP in CA1 hippocampal neurons.
Article in Pflugers Archiv : European journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 48 citations in OpenAlex.
- Advances in calcium signalling research for the diagnosis and treatment of depression.Annals of medicine · 2026Review
- Temperature and intrinsic CaNature structural & molecular biology · 2026Article
- Modulation of NMDA Receptor and TRPM4 Activity in Hippocampal Neurons with the NMDA Receptor/TRPM4 Interface Inhibitor Brophenexin.Neurotoxicity research · 2026Article
- Robust Hippocampal Synaptic Plasticity Despite Gut Microbiota Depletion in Adult Mice.The European journal of neuroscience · 2025Article
- The TRP channels serving as chemical-to-electrical signal converter.Physiological reviews · 2025Review
- TRP Channels in Excitotoxicity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025Review
- NMDA Receptor-Mediated CaPharmacology research & perspectives · 2024Article
- Article
- TRPM4 regulates hilar mossy cell loss in temporal lobe epilepsy.BMC biology · 2023Article
- Intracellular CaFrontiers in physiology · 2023Review
- Defining the role of TRPM4 in broadly responsive taste receptor cells.Frontiers in cellular neuroscience · 2023Article
- A glibenclamide-sensitive TRPM4-mediated component of CA1 excitatory postsynaptic potentials appears in experimental autoimmune encephalomyelitis.Scientific reports · 2022Article
- The short form of the SUR1 and its functional implications in the damaged brain.Neural regeneration research · 2022Review
- Computational models of neurotransmission at cerebellar synapses unveil the impact on network computation.Frontiers in computational neuroscience · 2022Review
- Pharmacological Modulation and (Patho)Physiological Roles of TRPM4 Channel-Part 2: TRPM4 in Health and Disease.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Microbial memories: Sex-dependent impact of the gut microbiome on hippocampal plasticity.The European journal of neuroscience · 2021Article
- TRPV4 Regulates Soman-Induced Status Epilepticus and Secondary Brain Injury via NMDA Receptor and NLRP3 Inflammasome.Neuroscience bulletin · 2021Article
- Elevating the Levels of Calcium Ions Exacerbate Alzheimer's Disease via Inducing the Production and Aggregation of β-Amyloid Protein and Phosphorylated Tau.International journal of molecular sciences · 2021Review
- IInternational journal of molecular sciences · 2021Article
- TRPM3 in Brain (Patho)Physiology.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TRPM4 is a calcium-activated but calcium-impermeable non-selective cation (CAN) channel. Previous studies have shown that TRPM4 is an important regulator of Ca(2+)-dependent changes in membrane potential in excitable and non-excitable cell types. However, its physiological significance in neurons of the central nervous system remained unclear. Here, we report that TRPM4 proteins form a CAN channel in CA1 neurons of the hippocampus and we show that TRPM4 is an essential co-activator of N-methyl-D-aspartate (NMDA) receptors (NMDAR) during the induction of long-term potentiation (LTP). Disrupting the Trpm4 gene in mice specifically eliminates NMDAR-dependent LTP, while basal synaptic transmission, short-term plasticity, and NMDAR-dependent long-term depression are unchanged. The induction of LTP in Trpm4 (-/-) neurons was rescued by facilitating NMDA receptor activation or post-synaptic membrane depolarization. Accordingly, we obtained normal LTP in Trpm4 (-/-) neurons in a pairing protocol, where post-synaptic depolarization was applied in parallel to pre-synaptic stimulation. Taken together, our data are consistent with a novel model of LTP induction in CA1 hippocampal neurons, in which TRPM4 is an essential player in a feed-forward loop that generates the post-synaptic membrane depolarization which is necessary to fully activate NMDA receptors during the induction of LTP but which is dispensable for the induction of long-term depression (LTD). These results have important implications for the understanding of the induction process of LTP and the development of nootropic medication.
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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.