Brain-derived neurotrophic factor (BDNF) is an important neurotrophin for the regulation of synaptic activity. BDNF-TrkB signaling, TrkB being the receptor of BDNF, is involved in transcription, translation, and trafficking of proteins in the various stages of synaptic development and evidence indicates that it also plays a significant role in synaptic plasticity, the ability of synapses to strengthen or weaken over time. Synaptic plasticity has been associated with learning and memory development. These functions are carried out through three pathways: mitogen-activated protein kinase (MAPK), phospholipase CG (PLC/PLCG), and phosphatidylinositol 3-kinase (PI3K). Pi3K and MAPK have crucial roles in the protein translation and transport caused by synaptic activity. PLCG regulates intracellular levels of Ca2+, which drives gene transcription through cyclic AMP. Evidence strongly indicates that abnormal levels of BDNF leads to significant developmental and neurodegenerative diseases by disrupting neural development and function. An understanding of how the BDNF-TrkB pathway regulates synaptic activity and plasticity is essential to an understanding of how we can effectively treat genetic disruptions of this pathway that lead to terrible neurodevelopmental diseases.
Proteins on this pathway have targeted assays available via the [CPTAC Assay Portal](https://assays.cancer.gov/available_assays?wp_id=WP3676).