The initiation of intracellular signaling cascades following the binding of a neurotrophic factor, such as BDNF or NGF, to its specific, high-affinity transmembrane receptor on the neuronal surface. This activation is the essential molecular event that dictates neuronal survival, guides differentiation, and promotes the structural plasticity of synapses. It is a foundational mechanism for maintaining and restoring brain health.
Origin
This term is a precise description from molecular neurobiology, combining ‘Neurotrophin’ (nerve nourishment) with ‘Receptor Activation’, the core event of ligand-receptor binding. The Trk family of receptors (TrkA, TrkB, TrkC) are the canonical high-affinity receptors that mediate these critical cellular responses.
Mechanism
Upon the binding of the neurotrophin ligand, the receptor dimerizes, and its intrinsic tyrosine kinase domain undergoes autophosphorylation and subsequent activation. This activation initiates parallel signaling pathways, including the Ras/MAPK cascade for differentiation and the PI3K/Akt pathway for anti-apoptotic survival signaling. The resulting intracellular signals modulate gene expression and protein synthesis, thereby ensuring the long-term structural and functional integrity of the neuron.
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