ArticleMolecular neurobiology2020
Inverse Agonism of Cannabinoid Receptor Type 2 Confers Anti-inflammatory and Neuroprotective Effects Following Status Epileptics.
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Development of highly potent EP2 antagonists as novel anti-inflammatory neuroprotectants.Bioorganic & medicinal chemistry · 2026Article
- Status epilepticus-induced 12/15-lipoxygenase drives neuroinflammation and contributes to neuronal injuries and behavioral comorbidities.Acta pharmacologica Sinica · 2026Article
- Pathophysiological roles of neural stem cells in neuropsychiatric diseases: from plasticity to pharmacological targeting.Acta pharmacologica Sinica · 2026Review
- Antiseizure Effects of Mirtazapine in a Rat Model of Status Epilepticus Via Cannabinoid Receptor Modulation.Neurochemical research · 2025Article
- Cannabinoid Receptor 2 (CB2) in Macrophages: A Promising Clinical Target for Immune Disorders.International journal of molecular sciences · 2025Review
- Suppressing the Inflammatory Prostaglandin Signaling after Thrombotic Stroke Ameliorates Ischemic Brain Injury and Facilitates Poststroke Recovery.ACS pharmacology & translational science · 2024Article
- Cell-specific NFIA upregulation promotes epileptogenesis by TRPV4-mediated astrocyte reactivity.Journal of neuroinflammation · 2023Article
- Exploring the Therapeutic Potential of Cannabinoid Receptor Antagonists in Inflammation, Diabetes Mellitus, and Obesity.Biomedicines · 2023Review
- Transient inhibition of microsomal prostaglandin E synthase-1 after status epilepticus blunts brain inflammation and is neuroprotective.Molecular brain · 2023Article
- Enhancing axonal myelination in seniors: A review exploring the potential impact cannabis has on myelination in the aged brain.Frontiers in aging neuroscience · 2023Review
- TRPC channels as emerging targets for seizure disorders.Trends in pharmacological sciences · 2022Review
- Ablation of Siglec-E augments brain inflammation and ischemic injury.Journal of neuroinflammation · 2022Article
- Inhibition of TRPC3 channels by a novel pyrazole compound confers antiseizure effects.Epilepsia · 2022Article
- Editorial: Cannabinoids in neuroinflammation, neurodegeneration and pain: Focus on non-neuronal cells.Frontiers in neuroscience · 2022Article
- Inducible Prostaglandin E Synthase as a Pharmacological Target for Ischemic Stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- The Endocannabinoid System in Glial Cells and Their Profitable Interactions to Treat Epilepsy: Evidence from Animal Models.International journal of molecular sciences · 2021Review
- Neuroinflammation in neurological disorders: pharmacotherapeutic targets from bench to bedside.Metabolic brain disease · 2021Review
- EP2 Antagonists (2011-2021): A Decade's Journey from Discovery to Therapeutics.Journal of medicinal chemistry · 2021Review
- Article
- Endocannabinoid-Mediated Control of Neural Circuit Excitability and Epileptic Seizures.Frontiers in neural circuits · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Prolonged status epilepticus (SE) in humans causes high mortality and brain inflammation-associated neuronal injury and morbidity in survivors. Currently, the only effective treatment is to terminate the seizures swiftly to prevent brain damage. However, reliance on acute therapies alone would be imprudent due to the required short response time. Follow-on therapies that can be delivered well after the SE onset are in an urgent need. Cannabinoid receptor type 2 (CB2), a G protein-coupled receptor that can be expressed by activated brain microglia, has emerged as an appealing anti-inflammatory target for brain conditions. In the current study, we reported that the CB2 inverse agonism by our current lead compound SMM-189 largely prevented the rat primary microglia-mediated inflammation and showed moderate neuroprotection against N-methyl-D-aspartic acid (NMDA) receptor-mediated excitotoxicity in rat primary hippocampal cultures containing both neurons and glia. Using a classical mouse model of epilepsy, in which SE was induced by systemic administration of kainate (30 mg/kg, i.p.) and proceeded for 1 h, we demonstrated that SE downregulated the CB1 but slightly upregulated CB2 receptor in the hippocampus. Transient treatment with SMM-189 (6 mg/kg, i.p., b.i.d.) after the SE was interrupted by diazepam (10 mg/kg, i.p.) prevented the seizure-induced cytokine surge in the brain, neuronal death, and behavioral impairments 24 h after SE. Our results suggest that CB2 inverse agonism might provide an adjunctive anti-inflammatory therapy that can be delivered hours after SE onset, together with NMDA receptor blockers and first-line anti-convulsants, to reduce brain injury and functional deficits following prolonged seizures.
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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.