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12 items found for "Neuroinflammation"
Posts (9)
- Chemogenetic stimulation of the G i pathway in astrocytes suppresses neuroinflammation
In this study, we evaluated the role of the astrocytic Gi pathway in neuroinflammation using a Gi -coupled Gi -DREADD was expressed in hippocampal astrocytes of a lipopolysaccharide (LPS)-induced neuroinflammation We found that astrocyte Gi -DREADD stimulation using clozapine N-oxide (CNO) inhibits neuroinflammation Taken together, our results indicate that the astrocytic Gi pathway plays an inhibitory role in neuroinflammation , providing an opportunity to identify potential cellular and molecular targets to control neuroinflammation
- The microglial endocannabinoid system similarly regulated by lipopolysaccharide and interferon gamma
respond to cannabinoids which has implications for the development of cannabinoid-based treatments for neuroinflammation
- 📰 GPCR Weekly News, August 14 to 20, 2023
Disorders GPCRs in Oncology and Immunology Exacerbating effects of single-dose acute ethanol exposure on neuroinflammation
Other Pages (3)
- Exacerbating effects of single-dose acute ethanol exposure on neuroinflammation and amelioration by GPR110 (ADGRF1) activation
News < GPCRs in Oncology and Immunology Exacerbating effects of single-dose acute ethanol exposure on neuroinflammation and amelioration by GPR110 (ADGRF1) activation Published date August 14, 2023 Abstract "Background: Neuroinflammation pharmacological activation of GPR110 in both central and peripheral immune cells cooperatively ameliorates neuroinflammation
- Unbiased multitissue transcriptomic analysis reveals complex neuroendocrine regulatory networks mediated by spinal cord injury-induced immunodeficiency
Progressive neuroinflammation spreads after injury, and neurotransmission through Gi-mediated G protein-coupled Zhou , Jin-Wu Wang Tags Hypothalamo-pituitary-adrenal axis , Neuroendocrine immunomodulatory axis , Neuroinflammation
- Posters | Adhesion GPCR Workshop 2024 | Dr. GPCR Ecosystem
ligand-induced signaling causes object recognition and spatial memory deficits in adulthood and increased neuroinflammatory gene expression for neuronal differentiation, axonogenesis, and synaptogenesis, as well as altered neuroinflammatory