[P2.67]: Effective protection of neural progenitor cells by olfactory ensheathing cells via phosphatidylinositol 3‐kinase/akt signaling on exposure to 6‐hydroxydopamine

asked whether Sema3A/F’s growth-suppressive actions required BDNF. Indeed, treatment with a function-blocking BDNF antibody suppressed Sema3A/F-induced growth cone collapse, suggesting that sempahorin requires ligand-induced activation of p75NTR for its biological activity. To identify the signaling pathway mediating Sema3A/F-p75NTR-induced growth cone collapse, we examined the role of the RhoA effector ROCK, which is required for the growth suppressive activity of p75NTR. Pharmacological inhibition of ROCK suppressed Sema3A/F-mediated axon growth collapse. We propose that BDNF-activated p75NTR and p75NTR-RhoAROCK signaling is necessary for semaphorin’s growth suppressive effects in sympathetic neurons. p75NTR may act either in a complex with semaphorin receptors, or as a ligand-activated receptor whose activity is required for semaphorin to induce its effects.