ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Transient receptor potential channel activation causes a novel form of [Ca 2+]I oscillations and is not involved in capacitative Ca 2+ entry in glial cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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Who cites it
36 citing papers in PubMed, 93 citations in OpenAlex.
- Revisiting astrocytic calcium signaling in the brain.Fundamental research · 2024Review
- Extracellular Calcium Influx Pathways in Astrocyte Calcium Microdomain Physiology.Biomolecules · 2021Review
- Cytosolic CaTheranostics · 2021Article
- Physiology of Astroglia.Advances in experimental medicine and biology · 2019Review
- Physiology of Astroglia.Physiological reviews · 2018Review
- TRPC3/6/7 Knockdown Protects the Brain from Cerebral Ischemia Injury via Astrocyte Apoptosis Inhibition and Effects on NF-кB Translocation.Molecular neurobiology · 2017Article
- TRPC1- and TRPC3-dependent CaGlia · 2017Article
- Diversity of Evoked Astrocyte CaFrontiers in systems neuroscience · 2017Article
- TRP channels in oxygen physiology: distinctive functional properties and roles of TRPA1 in OProceedings of the Japan Academy. Series B, Physical and biological sciences · 2017Review
- Beyond neurovascular coupling, role of astrocytes in the regulation of vascular tone.Neuroscience · 2016Review
- Store-Operated Calcium Entry in Müller Glia Is Controlled by Synergistic Activation of TRPC and Orai Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- STIM and ORAI proteins in the nervous system.Channels (Austin, Tex.) · 2015Review
- The deadly connection between endoplasmic reticulum, Ca2+, protein synthesis, and the endoplasmic reticulum stress response in malignant glioma cells.Neuro-oncology · 2014Article
- Store-operated calcium entry in neuroglia.Neuroscience bulletin · 2014Review
- Dopaminergic neurotoxicants cause biphasic inhibition of purinergic calcium signaling in astrocytes.PloS one · 2014Article
- TRP channels coordinate ion signalling in astroglia.Reviews of physiology, biochemistry and pharmacology · 2014Review
- Store-operated Ca2+ channels blockers inhibit lipopolysaccharide induced astrocyte activation.Neurochemical research · 2013Article
- TRPC1-mediated Ca2+ and Na+ signalling in astroglia: differential filtering of extracellular cations.Cell calcium · 2013Article
- Sulindac sulfide inhibits sarcoendoplasmic reticulum Ca2+ ATPase, induces endoplasmic reticulum stress response, and exerts toxicity in glioma cells: relevant similarities to and important differences from celecoxib.Journal of neuroscience research · 2013Article
- Manganese inhibits ATP-induced calcium entry through the transient receptor potential channel TRPC3 in astrocytes.Neurotoxicology · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Astrocytes express transient receptor potential channels (TRPCs), which have been implicated in Ca 2+ influx triggered by intracellular Ca 2+ stores depletion, a phenomenon known as capacitative Ca 2+ entry. We studied the properties of capacitative Ca 2+ entry in astrocytes by means of single-cell Ca 2+ imaging with the aim of understanding the involvement of TRPCs in this function. We found that, in astrocytes, capacitative Ca 2+ entry is not attributable to TRPC opening because the TRPC-permeable ions Sr2+ and Ba2+ do not enter astrocytes during capacitative Ca 2+ entry. Instead, natively expressed oleyl-acetyl-glycerol (OAG) (a structural analog of DAG) -sensitive TRPCs, when activated, initiate oscillations of cytosolic Ca 2+ concentration ([Ca 2+]i) pharmacologically and molecularly consistent with TRPC3 activation. OAG-induced [Ca 2+]i oscillations are not affected by inhibition of inositol trisphosphate (InsP3) production or blockade of the InsP3 receptor, therefore representing a novel form of [Ca 2+]i signaling. Instead, high [Ca 2+]i inhibited oscillations, by closing the OAG-sensitive channel. Also, treatment of astrocytes with antisense against TRPC3 caused a consistent decrease of the cells responding to OAG. Exogenous OAG but not endogenous DAG seems to activate TRPC3. In conclusion, in glial cells, natively expressed TRPC3s mediates a novel form of Ca 2+ signaling, distinct from capacitative Ca 2+ entry, which suggests a specific signaling function for this channel in glial cells.
Indexed as
Identifiers
12805313PMC6740795W1576543894What OpenQuestion holds
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.