trkb receptor การใช้

• BDNF released from microglia induces neuronal hyperexcitability through interaction with the TrkB receptor.
• The TrkB receptor is part of the large family of receptor tyrosine kinases.
• BDNF can function as a chemotactic factor for neural precursors during migration by activating TrkB receptors.
• After its activation, BDNF binds TrkB receptors whose subsequent activation results in dimerization and autophosphorylation of the receptor.
• In a similar study on a mouse mutant with reduced expression of trkB receptors, LTP of CA1 cells reduced significantly.
• While the TrkB receptor interacts with BDNF in a ligand-specific manner, all neurotrophins can interact with the p75 receptor.
• Numb binds to TrkB receptors to act as an endocytic regulator of TrkB and promote aPKC activation by acting as a scaffolding protein.
• KCC2 is transcriptionally downregulated following central nervous system injury by the TrkB receptor signalling transduction cascade ( activated by BDNF and NT-4 / 5 ).
• Local interaction of BDNF with the TrkB receptor on a single dendritic segment is able to stimulate an increase in PSD-95 trafficking to other separate dendrites as well as to the synapses of locally stimulated neurons.
• In addition, 7, 8-DHF possesses powerful antioxidant activity independent of its actions on the TrkB receptor, and protects against glutamate-induced excitotoxicity, 6-hydroxydopamine-induced dopaminergic neurotoxicity, and oxidative stress-induced genotoxicity.
• The TrkB receptor is encoded by the NTRK2 gene and is member of a receptor family of tyrosine kinases that includes TrkA and TrkC . TrkB autophosphorylation is dependent upon its ligand-specific association with BDNF, a widely expressed activity-dependent neurotic factor that regulates hypoxic injury.
• In its phosphorylated form, TrkB receptors recruit and bind adaptor proteins which result in the activation of MAPK . As described previously, MAPK pathways activate CREB . Thus, a feed-forward mechanism leads to the ramping up of p-CREB, BDNF, and TrkB levels which leads to the creation of new set-point, higher stimulus requirements to elicit a response, and may contribute to the downward spiral of alcoholism.