Brain-Derived Neurotrophic Factor and Its Potential Therapeutic Role in Stroke Comorbidities

Figure 3

Activation of the TrkB receptor by specific agonists triggers downstream signaling cascades to induce transcription and suppress apoptosis. Upon binding to the TrkB receptor, specific agonistic agents induce the formation of a TrkB homodimer and autophosphorylation of the intracellular tyrosine kinase domains, as well as the activation of the PLCγ (phospholipase C gamma), MAPK/ERK, and PI3K/Akt signaling pathways. While the latter two pathways suppress apoptosis by interacting with apoptosis-regulating proteins, such as BCL2, BAX, and Bad, all three pathways activate CREB-mediated transcription of prosurvival genes and thus protect neurons from apoptosis.