ArticleMolecular neurobiology2021
CB2 receptors modulate seizure-induced expression of pro-inflammatory cytokines in the hippocampus but not neocortex.
Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 15 citations in OpenAlex.
- Cannabinoid Receptor-2 Alleviates Sepsis-Induced Neuroinflammation by Modulating Microglia M1/M2 Subset Polarization Through Inhibiting Nogo-B Expression.Molecular neurobiology · 2025Article
- Inflammatory response of leptomeninges to a single cortical spreading depolarization.The journal of headache and pain · 2024Article
- Pre-existingFrontiers in molecular neuroscience · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
We compared neuroinflammatory responses induced by nonconvulsive and convulsive seizures and analyzed the role that may be played by cannabinoid CB2 receptors in the neuroinflammatory response induced by generalized tonic-clonic seizures (GTCS). Using quantitative PCR, we analyzed expression of interleukin-1b, CCL2, interleukin-6, tumor necrosis factor (TNF), transforming growth factor beta 1 (TGFb1), fractalkine, and cannabinoid receptor type 2 in the neocortex, dorsal and ventral hippocampus, cortical leptomeninges, dura mater, and spleen in 3 and 6 h after induction of GTCS by a high dose of pentylenetetrazole (PTZ, 70 mg/kg) and absence-like activity by a low dose of PTZ (30 mg/kg). The low dose of PTZ had no effect on the gene expression 3 and 6 h after PTZ injection. In 3 and 6 h after high PTZ dose, the expression of CCL2 and TNF increased in the neocortex. Both ventral and dorsal parts of the hippocampus responded to seizures by elevation of CCL2 expression 3 h after PTZ. Cortical leptomeninges but not dura mater also had elevated CCL2 level and decreased TGFb1 expression 3 h after GTCS. Activation of CB2 receptors by HU308 suppressed an inflammatory response only in the dorsal hippocampus but not neocortex. Suppression of CB2 receptors by AM630 potentiated expression of inflammatory cytokines also in the hippocampus but not in the neocortex. Thus, we showed that GTCS, but not the absence-like activity, provoke inflammatory response in the neocortex, dorsal and ventral hippocampus, and cortical leptomeninges. Modulation of CB2 receptors changes seizure-induced neuroinflammation only in the hippocampus but not neocortex.
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