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[P2.67]: Effective protection of neural progenitor cells by olfactory ensheathing cells via phosphatidylinositol 3‐kinase/akt signaling on exposure to 6‐hydroxydopamine
Author(s) -
Seth K.,
Srivastava N.,
Ansari R.W.,
Agrawal A.K.
Publication year - 2008
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2008.09.192
Subject(s) - hydroxydopamine , olfactory ensheathing glia , protein kinase b , neural stem cell , progenitor cell , microbiology and biotechnology , phosphatidylinositol , kinase , pi3k/akt/mtor pathway , chemistry , olfactory system , neuroscience , signal transduction , biology , olfactory bulb , stem cell , central nervous system , dopamine , dopaminergic
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.