ArticleExperimental neurology2009
Protease-activated receptor 1-dependent neuronal damage involves NMDA receptor function.
Article in Experimental neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
34 citing papers in PubMed, 55 citations in OpenAlex.
- Effect of Physical Exercise on Acute Post-traumatic Hyperexcitability: The Role of Thrombin/PAR1 Signaling.Molecular neurobiology · 2026Article
- PAR-1 in Alzheimer's Disease: Pathophysiological Insights and Mechanistic Perspectives.Current medical science · 2026Review
- Super-high procoagulant activity of gecko thrombin: A gift from sky dragon.CNS neuroscience & therapeutics · 2023Article
- Inhibition of protease-activated receptor 1 (PAR1) ameliorates cognitive performance and synaptic plasticity impairments in animal model of Alzheimer's diseases.Psychopharmacology · 2021Article
- The thrombin receptor links brain derived neurotrophic factor to neuron cholesterol production, resiliency and repair after spinal cord injury.Neurobiology of disease · 2021Article
- Role of Thrombin in Central Nervous System Injury and Disease.Biomolecules · 2021Review
- Thrombin contributes to the injury development and neurological deficit after acute subdural hemorrhage in rats only in collaboration with additional blood-derived factors.BMC neuroscience · 2018Article
- MMP-1 overexpression selectively alters inhibition in D1 spiny projection neurons in the mouse nucleus accumbens core.Scientific reports · 2018Article
- Neuro-Immune Hemostasis: Homeostasis and Diseases in the Central Nervous System.Frontiers in cellular neuroscience · 2018Review
- Neuro-Coagulopathy: Blood Coagulation Factors in Central Nervous System Diseases.International journal of molecular sciences · 2017Review
- Astroglia as a cellular target for neuroprotection and treatment of neuro-psychiatric disorders.Glia · 2017Review
- Targeting PAR1: Now What?Trends in pharmacological sciences · 2017Review
- A Linear Temporal Increase in Thrombin Activity and Loss of Its Receptor in Mouse Brain following Ischemic Stroke.Frontiers in neurology · 2017Article
- Targeting the thrombin receptor modulates inflammation and astrogliosis to improve recovery after spinal cord injury.Neurobiology of disease · 2016Article
- Protective and detrimental effects of neuroectodermal cell-derived tissue factor in mouse models of stroke.JCI insight · 2016Article
- Protease activated receptor 1 (PAR1) enhances Src-mediated tyrosine phosphorylation of NMDA receptor in intracerebral hemorrhage (ICH).Scientific reports · 2016Article
- Stages of the Inflammatory Response in Pathology and Tissue Repair after Intracerebral Hemorrhage.Seminars in neurology · 2016Review
- Contribution of protease-activated receptor 1 in status epilepticus-induced epileptogenesis.Neurobiology of disease · 2015Article
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Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Protease-activated receptor 1 (PAR1) is a G-protein coupled receptor that is expressed throughout the central nervous system. PAR1 activation by brain-derived as well as blood-derived proteases has been shown to have variable and complex effects in a variety of animal models of neuronal injury and inflammation. In this study, we have evaluated the effects of PAR1 on lesion volume in wild-type or PAR1-/- C57Bl/6 mice subjected to transient occlusion of the middle cerebral artery or injected with NMDA in the striatum. We found that removal of PAR1 reduced infarct volume following transient focal ischemia to 57% of control. Removal of PAR1 or application of a PAR1 antagonist also reduced the neuronal injury associated with intrastriatal injection of NMDA to 60% of control. To explore whether NMDA receptor potentiation by PAR1 activation contributes to the harmful effects of PAR1, we investigated the effect of NMDA receptor antagonists on the neuroprotective phenotype of PAR1-/- mice. We found that MK801 reduced penumbral but not core neuronal injury in mice subjected to transient middle cerebral artery occlusion or intrastriatal NMDA injection. Lesion volumes in both models were not significantly different between PAR1-/- mice treated with and without MK801. Use of the NMDA receptor antagonist and dissociative anesthetic ketamine also renders NMDA-induced lesion volumes identical in PAR1-/- mice and wild-type mice. These data suggest that the ability of PAR1 activation to potentiate NMDA receptor function may underlie its harmful actions during injury.
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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.