Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Mar 19;12(3):379–392. doi: 10.5498/wjp.v12.i3.379

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/

PMC Copyright notice

Role of brain-derived neurotrophic factor and pro-BDNF in neuroimmune crosstalk in mood disorders. Brain-derived neurotrophic factor (BDNF) or pro-BDNF can be stored in the dense-core vesicles and released upon neuronal activity. The released BDNF and pro-BDNF mainly bind to their high affinity receptors, TrkB and p75^NTR, respectively and mediate the downstream signaling pathways. BDNF-TrkB signaling leads to neuronal survival, development and long-term potentiation. In contrast, pro-BDNF-p75^NTR signaling mediates neuronal apoptosis, axonal pruning and long-term depression. BDNF: Brain-derived neurotrophic factor; NF-κB: Nuclear factor-κB.