Objectives: To examine the effect of BDNF on F-actin during the stimulation of IL-1β in hippocampal neurons.
Materials & methods: We cultured hippocampal neurons from rat embryos. Cell stimulation was induced by IL-1β. Cell culture success was evaluated by an activity analysis of CCK-8, staining of gliocyte by immunohistochemistry. Changes in F-actin, BDNF and NF-ĸB were examined using molecular analyses.
Results: Our results demonstrate that a high concentration of IL-1β exaggerates the stimulation-induced degradation of F-actin by BDNF, whereas a low concentration of IL-1β protects F-actin against this degradation. These beneficial effects might be associated with the inhibition or exaggeration of the NF-ĸB signaling cascade.
Conclusions: Taken together, our findings indicate that BDNF acts as an F-actin-protective regulator during stimulation by IL-1β and that this function largely occurs via the regulation of NF- ĸB signaling. These results suggest that interventions targeting the BDNF signaling system may be of therapeutic value against major depressive disorder (MDD).