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Updated: Jan 31, 2026

Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates
Published on: March 20, 2014
Role of Kinin B2 Receptor Signaling in Astrocyte-driven Neuroinflammation
Mariana R Tavares1, Gabriel R Estrela2, Luana Lavezo1
1Department of Neurology and Neurosurgery, Federal University of Sao Paulo, Sao Paulo, 04039-032, Brazil.
None:
The kallikrein-kinin system (KKS) plays a key role in inflammatory responses, but its specific contribution to neuroinflammation remains to be fully elucidated. The bradykinin B2 receptor (B2R), a principal effector of the KKS, is widely expressed in both neuronal and glial cells in the rodent and human brain. In this study, we investigated the molecular contribution of B2R to neuroinflammation using complementary in vitro and in vivo models. Lipopolysaccharide (LPS) stimulation significantly upregulated B2R mRNA expression in primary astrocyte cultures and in the cortical tissue of wild-type mice. Pharmacological blockade of B2R in astrocytes markedly suppressed the LPS-induced proinflammatory gene expression. In contrast, B2R antagonism in vivo resulted in only partial attenuation of the neuroinflammatory response. Together, these findings suggest cell type-specific roles for B2R and underscore its key contribution to astrocyte-mediated neuroinflammation.
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