ArticleThe Journal of general physiology2009
Intracellular calcium strongly potentiates agonist-activated TRPC5 channels.
Article in The Journal of general physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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Who cites it
98 citing papers in PubMed, 153 citations in OpenAlex.
- Transient receptor potential canonical (TRPC) channels in diabetes and associated complications.Channels (Austin, Tex.) · 2026Review
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Structure-guided design of picomolar-level macrocyclic TRPC5 channel inhibitors with antidepressant activity.Acta pharmaceutica Sinica. B · 2026Article
- Direct crosstalk between GPCRs and ion channels via G proteins.Experimental & molecular medicine · 2025Review
- Physiological functions and pharmacological targeting of transient receptor potential channels.Pharmacological reviews · 2025Review
- TRPC4/5 inhibitors: Phase I results and proof of concept studies.European archives of psychiatry and clinical neuroscience · 2025Review
- Thermo-TRP regulation by endogenous factors and its physiological function at core body temperature.Physiological reports · 2025Review
- Article
- TRPC5 controls the adrenaline-mediated counter regulation of hypoglycemia.The EMBO journal · 2024Article
- Rap1A Modulates Store-Operated Calcium Entry in the Lung Endothelium: A Novel Mechanism Controlling NFAT-Mediated Vascular Inflammation and Permeability.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Thermosensing ability of TRPC5: current knowledge and unsettled questions.The journal of physiological sciences : JPS · 2024Review
- Estradiol elicits distinct firing patterns in arcuate nucleus kisspeptin neurons of females through altering ion channel conductances.bioRxiv : the preprint server for biology · 2024Article
- Functions of TRPs in retinal tissue in physiological and pathological conditions.Frontiers in molecular neuroscience · 2024Review
- The SphK1/S1P Axis Regulates Synaptic Vesicle Endocytosis via TRPC5 Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Molecular architecture of the GαNature communications · 2023Article
- Negative self-regulation of transient receptor potential canonical 4 by the specific interaction with phospholipase C-δ1.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- TRPC1 channel clustering during store-operated CaFrontiers in physiology · 2023Article
- TRPC channels as emerging targets for seizure disorders.Trends in pharmacological sciences · 2022Review
- The interplay between physical cues and mechanosensitive ion channels in cancer metastasis.Frontiers in cell and developmental biology · 2022Review
- Deletion ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
TRPC5 is a calcium (Ca(2+))-permeable nonselective cation channel expressed in several brain regions, including the hippocampus, cerebellum, and amygdala. Although TRPC5 is activated by receptors coupled to phospholipase C, the precise signaling pathway and modulatory signals remain poorly defined. We find that during continuous agonist activation, heterologously expressed TRPC5 currents are potentiated in a voltage-dependent manner ( approximately 5-fold at positive potentials and approximately 25-fold at negative potentials). The reversal potential, doubly rectifying current-voltage relation, and permeability to large cations such as N-methyl-d-glucamine remain unchanged during this potentiation. The TRPC5 current potentiation depends on extracellular Ca(2+): replacement by Ba(2+) or Mg(2+) abolishes it, whereas the addition of 10 mM Ca(2+) accelerates it. The site of action for Ca(2+) is intracellular, as simultaneous fura-2 imaging and patch clamp recordings indicate that potentiation is triggered at approximately 1 microM [Ca(2+)]. This potentiation is prevented when intracellular Ca(2+) is tightly buffered, but it is promoted when recording with internal solutions containing elevated [Ca(2+)]. In cell-attached and excised inside-out single-channel recordings, increases in internal [Ca(2+)] led to an approximately 10-20-fold increase in channel open probability, whereas single-channel conductance was unchanged. Ca(2+)-dependent potentiation should result in TRPC5 channel activation preferentially during periods of repetitive firing or coincident neurotransmitter receptor activation.
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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.