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TRKBTropomyosin-Related Kinase B
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To observe changes in expression levels of BDNF and TrkB proteins in the DG, six mice from each group were anesthetized with Zoletil 50[R] (30 mg/kg) and sacrificed by cervical dislocation.
Conclusion: Voluntary exercise in different levels potentiates the brain rewarding system, CPP scale, and hippocampal BDNF and TrKB expressions.
BDNF stimulates TrkB receptors of lamina I secondary sensory neurons in dorsal horn to cause down-regulation of the potassium-chloride transporter KCC2, resulting in an increase in intracellular [[Cl.
TrkB signaling in retinal glia stimulates neuroprotection after optic nerve injury.
We have reported that the TrkB agonist 7,8-dihydroxyflavone (7,8-DHF) attenuates behavioural abnormalities (such as hyperlocomotion and prepulse inhibition deficits) in mice after administration of METH and that 7,8-DHF attenuates the development of behavioural sensitisation and dopaminergic neurotoxicity in mice after repeated administration of METH.
Abnormality in the way BDNF communicates with the receptor TrkB leads to impaired poor cardiac function.
Effect of 7,8-Dihydroxyfavone, a Small-Molecule TrkB Agonist, on Emotional Learning.
TrkB phosphorylation by Cdk5 is required for activity-dependent structural plasticity and spatial memory.
Conditional deletion of TrkB but not BDNF prevents epileptogenesis in the kindling model.
Amygdala kindling was impaired in BDNF knockout mice [47, 48] or by intraventricular infusion of "TrkB receptor bodies" [49], and was abolished in conditional TrkB knockouts [48].