Kainic Acid-Induced Neurodegenerative Model: Potentials and Limitations

Figure 2

KA-induced microglial activation. Activated microglia express MHC class I and II, costimulatory molecules (CD80 and CD86), chemokine receptors (CCR2, 3, 5, CXCR3, 4, etc.), cytokine receptors (IL-10R, IL-12R, IL-18R, IFNgR, TNFR, TGFβR, etc.), complement receptors (FCγRI-III and CR1, 3, 4, etc.), and prostaglandin receptors, produce complements, prostaglandins, cytokines (IL-1, IL-6, IL-10, IL-12, IL-18, TNF-α, TGF-β, etc.), chemokines (IP-10, MIP-1α, MIP-1β, MCP-1, IL-8, RANTES, etc.), ROS, and RNS, and secrete neutrophins (NGF, BDNF, and NT-3, 4, etc.), proteases, and excitatory amino acids, and so forth, which may either contribute to excitotoxic damage or be protective against KA damage. IL: interleukin; CCR: C-C chemokine receptor; CXCR: CXC chemokine receptor; IFNgR: interferon gamma receptor; TNF: tumor necrosis factor; TGF: transforming growth factor; IP: Interferon gamma-inducible protein; MIP: macrophage inflammatory protein; MCP: monocyte chemotactic protein; RANTES: regulated upon activation, normal T-cell expressed and presumably secreted; NGF: nerve growth factor; BDNF: brain-derived neurotrophic factor; NT: neurotrophin.