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. 2022 Jul 12;13:917527. doi: 10.3389/fneur.2022.917527

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Copyright © 2022 Schirò, Iacono, Ragonese, Aridon, Salemi and Balistreri.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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TrkB and p75NTR signaling. The binding between BDNF and TrkB induces the activation of three transduction pathways at the intracellular level mediating their effects on neuronal growth and synaptic plasticity. The interaction between pro-BDNF and p75NTR receptor promotes cell apoptosis and neuronal survival via JNK NF-kB, respectively. BDNF, brain-derived neurotrophic factor; TrkB, tropomyosin receptor kinase; p75NTR, p75 neurotrophin receptor; Shc, Grb2, growth factor receptor-bound protein 2; SOS, Son of Sevenless; Gab1, GRB2-associated-binding protein 1; AKT, protein kinase B; PI3K, phosphatidylinositol 3-kinase; PLC, phospholipase C; PKC, protein kinase C; DAG, diacylglycerol; IP3, inositol-3-phosphate; CaMKII, type II calcium/calmodulin-dependent protein kinase; JNK, c-Jun N-terminal kinases; NF-kB, nuclear factor kappa B; CREB, cAMP response element-binding protein; mTOR, mammalian target of rapamycin; AMPA, α-Ammino-3-idrossi-5-Metil-4-isossazol-Propionic Acid.