Background: Appropriate mitochondrial transport and localization are highly associated with neuronal activities. Results: BDNF induces mitochondrial motility arrest via Miro1 binding with Ca 2ϩ , which facilitates BDNF-enhanced neurotransmitter release. Conclusion: BDNF-regulated mitochondrial motility is essential for BDNF-enhanced synaptic transmission. Significance: These results provide novel insights into the mechanistic link between BDNF-dependent mitochondrial motility and BDNF-mediated synaptic transmission.

Background: BDNF promotes axonal outgrowth, whereas the underlying molecular mechanism has remained unclear. Results: LIMK1 interacts with TrkB, and BDNF treatment could induce LIMK1 dimerization and transactivation, which facilitate axonal elongation. Conclusion: LIMK1-regulated actin dynamics is essential for BDNF-induced axonal elongation. Significance: These results revealed a novel mechanism for the BDNF-induced axonal elongation.

Background:Proper cell surface location of TrkA is crucial for NGF-mediated functions; however, the mechanisms modulating TrkA surface levels remain unclear. Results: Syntaxin 8 increases TrkA surface levels and modulates inflammatory pain transmission. Conclusion: Syntaxin 8-regulated TrkA surface targeting is essential for NGF-mediated functions. Significance: These findings advance our understanding of the mechanisms of TrkA surface targeting and pain transmission.