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. 2021 Nov 22;59(2):950–967. doi: 10.1007/s12035-021-02628-y

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — BDNF-TrkB- and GDNF-Gfrα-dependent signaling pathways. BDNF binds to receptor TrkB and activates three major signaling pathways [6]: PI3K/Akt; PLC/CAMK and PLC/PKC; Ras/ERK pathways. GDNF binds to its high-affinity receptor Gfrα and activates mainly PI3K/Akt; PLC/PKC and Rac1/Cdc42 signaling pathways [17, 18]. BDNF, brain-derived neurotrophic factor; TrkB, tropomyosin-related kinase B; PI3k, phosphoinositide 3-kinase; PDK1, phosphoinositide-dependent kinase-1; Akt, protein kinase B; PLCγ, phospholipase Cγ; IP3, inositol trisphosphate; CAMK, calcium/calmodulin-dependent kinase; DAG, diacylglycerol; PKC, protein kinase C; Raf, proto-oncogene serine/threonine-protein kinase; MEK, mitogen-activated protein kinase; GDNF, glial cell–derived neurotrophic factor; Gfrα, GDNF family receptor alpha; ERK, extracellular signal-regulated kinase 1/2; Rac1, Ras-related C3 botulinum toxin substrate 1; Cdc42, cell division control protein 42