Fig. (4).

Schematic outline for the proposed use of TrkB ligands as novel therapeutic drugs in depression. In preclinical studies, inflammation promotes reduced BDNF in the PFC and hippocampus, as well as increased BDNF in the NAc of the brain, resulting in a depression-like phenotype in rodents. From preclinical data, we propose that TrkB agonists and current antidepressants, such as SSRIs and SNRIs could be effective therapeutic drugs for depressed patients with decreased levels of BDNF in the PFC and hippocampus. In contrast, TrkB antagonists confer potential therapeutic benefits for patients with treatment-resistant depression showing increased BDNF levels in the VTA-NAc pathway.