As a result of a large number of in vitro as well as in vivo experiments with rodents, brain-derived neurotrophic factor (BDNF) and its tyrosine kinase receptor TrkB are now widely appreciated to play major roles in brain function. There is also a growing appreciation that decreased BDNF signalling may be a significant component in a wide range of brain dysfunction in humans based on the discovery of mutations and polymorphisms in the corresponding genes. Human neurons generated in vitro had been shown to be responsive to TrkB phosphorylation upon treatment with BNDF, TrkB agonist ZEB85, the related factor neurotrophin-4 (NT4). In order to compare the transcriptional changes upon treatment with the three TrkB ligands RNA-seq analysis was deployed. Cultures had been treated in triplicates with BDNF, ZEB85 or NT4 for 30 minutes, 2 hours, 12 hours and 24 hours, while non treated controls were lysed at each time-point.