ArticleFrontiers in molecular neuroscience2017
Protease Activated Receptor 2 (PAR2) Induces Long-Term Depression in the Hippocampus through Transient Receptor Potential Vanilloid 4 (TRPV4).
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Serum LBP and zonulin levels with brain MRS findings and gastrointestinal symptoms in schizophrenia and health.Brain, behavior, & immunity - health · 2026Article
- TRPV4 Channel in Neurological Disease: from Molecular Mechanisms to Therapeutic Potential.Molecular neurobiology · 2025Review
- Protease-activated receptors in health and disease.Physiological reviews · 2023Review
- Diversification of PAR signaling through receptor crosstalk.Cellular & molecular biology letters · 2022Review
- Discovery of Screening Biomarkers for Major Depressive Disorder in Remission by Proteomic Approach.Diagnostics (Basel, Switzerland) · 2021Article
- Emerging Roles of Protease-Activated Receptors (PARs) in the Modulation of Synaptic Transmission and Plasticity.International journal of molecular sciences · 2021Review
- Channels that Cooperate with TRPV4 in the Brain.Journal of molecular neuroscience : MN · 2020Review
- Planar coil-based contact-mode magnetic stimulation: synaptic responses in hippocampal slices and thermal considerations.Scientific reports · 2018Article
- Neuro-Coagulopathy: Blood Coagulation Factors in Central Nervous System Diseases.International journal of molecular sciences · 2017Review
- Neuroprotection induced by protease-activated receptor 2 activation is independent of Gq signalling.Brain and neuroscience advancesArticle
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protease activated receptors (PARs) are involved in regulating synaptic transmission and plasticity in the brain. While it is well-accepted that PAR1 mediates long-term potentiation (LTP) of excitatory synaptic strength, the role of PAR2 in synaptic plasticity remains not well-understood. In this study, we assessed the role of PAR2-signaling in plasticity at hippocampal Schaffer collateral-CA1 synapses. Using field potential recordings, we report that PAR2-activation leads to long-term depression (LTD) of synaptic transmission through a protein kinase A -dependent, Transient Receptor Potential Vanilloid 4 -mediated mechanism, which requires the activation of
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