ArticleNeuromolecular medicine2013
TRPC6 inhibited NMDA current in cultured hippocampal neurons.
Article in Neuromolecular medicine, 2013. 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, 24 citations in OpenAlex.
- Calcium Ions in the Physiology and Pathology of the Central Nervous System.International journal of molecular sciences · 2024Review
- TRP Channels in Stroke.Neuroscience bulletin · 2024Review
- Role of Neuronal TRPC6 Channels in Synapse Development, Memory Formation and Animal Behavior.International journal of molecular sciences · 2023Review
- Transient Receptor Potential Canonical 6 (TRPC6) Channel in the Pathogenesis of Diseases: A Jack of Many Trades.Inflammation · 2023Review
- Role of Calcium Modulation in the Pathophysiology and Treatment of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Protective effect of Achyranthes bidentata polypeptides on NMDA-mediated injury is developmentally regulated via modulating NR2A and NR2B differentially.Annals of translational medicine · 2021Article
- Review
- TRP Channels Regulation of Rho GTPases in Brain Context and Diseases.Frontiers in cell and developmental biology · 2020Review
- Novel Targets for Stroke Therapy: Special Focus on TRPC Channels and TRPC6.Frontiers in aging neuroscience · 2020Review
- TRPC6 Attenuates Cortical Astrocytic Apoptosis and Inflammation in Cerebral Ischemic/Reperfusion Injury.Frontiers in cell and developmental biology · 2020Article
- Cordycepin protects against β-amyloid and ibotenic acid-induced hippocampal CA1 pyramidal neuronal hyperactivity.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2019Article
- Knockdown of TRIM32 Protects Hippocampal Neurons from Oxygen-Glucose Deprivation-Induced Injury.Neurochemical research · 2019Article
- Heteromeric channels formed by TRPC1, TRPC4 and TRPC5 define hippocampal synaptic transmission and working memory.The EMBO journal · 2017Article
- TRPC6-mediated ERK1/2 Activation Regulates Neuronal Excitability via Subcellular Kv4.3 Localization in the Rat Hippocampus.Frontiers in cellular neuroscience · 2017Article
- Transient receptor potential channel 1/4 reduces subarachnoid hemorrhage-induced early brain injury in rats via calcineurin-mediated NMDAR and NFAT dephosphorylation.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-methyl-D-aspartate (NMDA) receptors play a key role in excitatory synaptic transmission, plasticity and neural development, and they also mediate excitotoxicity that is involved in both acute neuronal damage and chronic neurodegenerative diseases. Regulation of the NMDA channel activity is critical for the pathological processes of these diseases. The canonical transient receptor potential channels (TRPCs) are Ca(2+)-permeable nonselective cation channels with various physiological functions, including promoting neuronal survival. Here, we reported that TRPC6, a member of the TRPC family, inhibited the NMDA-induced current in primary cultured hippocampal neurons. Overexpression of TRPC6 or application of 1-oleoyl-2-acetyl-sn-glycerol, a compound known to activate TRPCs, inhibited the NMDA-induced current in these neurons assayed by the whole-cell patch-clamp recording. Consistently, downregulation of TRPC6 or application of SKF96365, a compound known to inhibit TRPCs, enhanced this current. The peak amplitude of the NMDA current in the neurons isolated from TRPC6 transgenic mice was greatly suppressed than that in the neurons isolated from the wild-type littermates. Furthermore, TRPC6 might activate calcineurin to inhibit the activity of NMDA receptors in cultured hippocampal neurons. Together, these results suggested that TRPC6 might be a novel negative modulator of NMDA receptors.
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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.