TrkB neurotrophin receptor at the core of antidepressant effects, but how?
Cell and tissue research July 1, 2019 Tomi Rantamäki
Brain-derived neurotrophic factor (BDNF) and its receptor TrkB have been studied for decades in mood disorders and their treatments. Various antidepressant drugs increase BDNF synthesis in the cortex, promoting neurotrophic processes and heightened plasticity. Induction of BDNF-TrkB signaling is also linked to ketamine and some anesthetics, even those without known antidepressant effects. Both ketamine and conventional antidepressants rapidly activate TrkB receptor signaling in the brain, while electroconvulsive therapy (ECT), a potent BDNF inducer, has not been clearly shown to produce such acute TrkB effects. Antidepressant regulation of TrkB signaling is developmentally regulated and requires an intact central nervous system. This review highlights peculiarities in how ketamine, classical antidepressants, and BDNF affect TrkB signaling.