Abstract
Accumulating evidence suggests that brain- derived neurotrophic factor (BDNF) and its receptor TrkB signaling plays a key role in the therapeutic mechanism of antidepressants. We found that BDNF-TrkB signaling was decreased in the prefrontal cortex and hippocampus from depressed rodents, whereas BDNF-TrkB signaling was increased in the nucleus accumbens from depressed rodents. TrkB agonist showed antidepressant effect via stimulation of TrkB signaling in the prefrontal cortex and hippocampus. In contrast, TrkB antagonist showed antidepressant effect via blockage of TrkB signaling in the nucleus accumbens. The N-methyl-D-aspartate (NMDA) receptor antagonist ketamine shows rapid antidepressant effects in treatment- resistant patients with major depression and bipolar depression. Here the author would like to discuss the role of BDNF-TrkB- mTOR signaling in the therapeutic mechanism of antidepressants and ketamine.
