ReviewJournal of molecular medicine (Berlin, Germany)2015
TRPC3-dependent synaptic transmission in central mammalian neurons.
Review in Journal of molecular medicine (Berlin, Germany), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Functional and structural basis of a hypermorphic TRPC3 variant.Science advances · 2026Article
- Heterogeneity in Slow Synaptic Transmission Diversifies Purkinje Cell Timing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- TRPC3 channel gating by lipids requires localization at the ER/PM junctions defined by STIM1.The Journal of cell biology · 2022Article
- TRPC3 Channel Activity and Viability of Purkinje Neurons can be Regulated by a Local Signalosome.Frontiers in molecular biosciences · 2022Article
- Ablation of polyamine catabolic enzymes provokes Purkinje cell damage, neuroinflammation, and severe ataxia.Journal of neuroinflammation · 2020Article
- Review
- Novel Targets for Stroke Therapy: Special Focus on TRPC Channels and TRPC6.Frontiers in aging neuroscience · 2020Review
- Disrupted Calcium Signaling in Animal Models of Human Spinocerebellar Ataxia (SCA).International journal of molecular sciences · 2019Review
- Human Brain Region-Specific Alternative Splicing of TRPC3, the Type 3 Canonical Transient Receptor Potential Non-Selective Cation Channel.Cerebellum (London, England) · 2019Article
- Article
- GABACells · 2018Article
- Control of neuronal excitability by Group I metabotropic glutamate receptors.Biophysical reviews · 2017Review
- Age-dependent alpha-synuclein accumulation is correlated with elevation of mitochondrial TRPC3 in the brains of monkeys and mice.Journal of neural transmission (Vienna, Austria : 1996) · 2017Article
- Receptors, G proteins, and integration of calcium signalling.Journal of molecular medicine (Berlin, Germany) · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transient receptor potential (TRPC) proteins form non-selective cation channels that are activated downstream of Gq-phospholipase C-coupled receptors. TRPC3, one of the seven members of the TRPC subfamily, combines functions of an unspecific ion channel and a signal transducer. In the mammalian brain, the expression of TRPC3 is highest in cerebellar Purkinje cells, the principal neurons, and the sole output of the cerebellar cortex. In this review, we summarize findings identifying TRPC3 channels as integral components of glutamatergic metabotropic synaptic transmission. We give an overview of postsynaptic interaction partners and activation mechanisms of TRPC3 in central neurons. Finally, we address the deleterious consequences of distorted TRPC3 synaptic signaling for cerebellar function in different mouse models and present TRPC3 as an emerging candidate protein implicated in various forms of ataxia in humans.
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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.