Abstract
Neuroscience Essentially, all antidepressant drugs increase the expression and signaling of brain-derived neurotrophic factor (BDNF). These drugs act through tyrosine kinase receptor 2 (TRKB), the receptor for BDNF, to regulate neuronal plasticity. Casarotto et al. investigated the potential interactions among TRKB, cholesterol, and antidepressants. The authors found that a dimer of TRKB forms a binding pocket, where several antidepressants from different drug classes bind with a low but physiologically meaningful affinity. This low-level binding depends on membrane cholesterol to stabilize the TRKB structure in synaptic membranes and thereby promotes BDNF signaling. Such direct binding to TRKB and promotion of BDNF-mediated plasticity may therefore be a common mechanism of action for anti-depressant drugs. Cell , 184 , 1299 (2021).
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
