PMID- 11553668 OWN - NLM STAT- MEDLINE DCOM- 20011025 LR - 20211203 IS - 0022-3042 (Print) IS - 0022-3042 (Linking) VI - 78 IP - 5 DP - 2001 Sep TI - Differences in survival-promoting effects and intracellular signaling properties of BDNF and IGF-1 in cultured cerebral cortical neurons. PG - 940-51 AB - Brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1) act on various neurons of the CNS as neurotrophic factors promoting neuronal differentiation and survival. We examined the survival-promoting effects of BDNF and IGF-1 on serum deprivation-induced death in cultured cerebral cortical neurons, and compared the intracellular signaling pathways stimulated by BDNF and IGF-1 in the neurons. We found that the survival-promoting effect of BDNF was much weaker than that of IGF-1 in serum deprivation-induced death of cultured cortical neurons. We found no differences in the levels of phosphatidylinositol 3-kinase (PtdIns3-K) activity or Akt (also called PKB) phosphorylation induced by BDNF and IGF-1 in the cultured cortical neurons, although many reports suggest that PtdIns3-K and Akt are involved in survival promotion. In addition, phosphorylation signals of mitogen-activated protein kinase (MAPK) and cAMP responsive element-binding protein (CREB), which have also been reported to be involved in survival promotion, were stimulated by BDNF much more potently than by IGF-1. These results show that there may be, as yet unidentified, intracellular signaling pathways other than the PtdIns3-K-Akt, MAPK and CREB signaling, to regulate survival promotion. These unidentified signaling pathways may be responsible for the distinct strengths of the survival-promoting effects of BDNF and IGF-1. FAU - Yamada, M AU - Yamada M AD - Institute for Protein Research, Osaka University, Osaka, Japan. yamada@protein.osaka-u.ac.jp FAU - Tanabe, K AU - Tanabe K FAU - Wada, K AU - Wada K FAU - Shimoke, K AU - Shimoke K FAU - Ishikawa, Y AU - Ishikawa Y FAU - Ikeuchi, T AU - Ikeuchi T FAU - Koizumi, S AU - Koizumi S FAU - Hatanaka, H AU - Hatanaka H LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - J Neurochem JT - Journal of neurochemistry JID - 2985190R RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Cyclic AMP Response Element-Binding Protein) RN - 0 (Proto-Oncogene Proteins) RN - 67763-96-6 (Insulin-Like Growth Factor I) RN - EC 2.7.10.2 (src-Family Kinases) RN - EC 2.7.11.1 (Akt1 protein, rat) RN - EC 2.7.11.1 (Protein Serine-Threonine Kinases) RN - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) SB - IM MH - Animals MH - Apoptosis/drug effects MH - Brain-Derived Neurotrophic Factor/*pharmacology MH - Cell Survival/drug effects MH - Cells, Cultured MH - Cerebral Cortex/cytology MH - Cyclic AMP Response Element-Binding Protein/metabolism MH - Female MH - Insulin-Like Growth Factor I/*pharmacology MH - MAP Kinase Signaling System/*drug effects MH - Male MH - Neurons/*cytology/*drug effects/enzymology MH - Phosphatidylinositol 3-Kinases/metabolism MH - *Protein Serine-Threonine Kinases MH - Proto-Oncogene Proteins/metabolism MH - Proto-Oncogene Proteins c-akt MH - Rats MH - Rats, Wistar MH - src-Family Kinases/metabolism EDAT- 2001/09/13 10:00 MHDA- 2001/10/26 10:01 CRDT- 2001/09/13 10:00 PHST- 2001/09/13 10:00 [pubmed] PHST- 2001/10/26 10:01 [medline] PHST- 2001/09/13 10:00 [entrez] AID - 10.1046/j.1471-4159.2001.00497.x [doi] PST - ppublish SO - J Neurochem. 2001 Sep;78(5):940-51. doi: 10.1046/j.1471-4159.2001.00497.x.