| Autor: |
Tohda, Chihiro, Hashimoto, Itsuki, Kuboyama, Tomoharu, Komatsu, Katsuko |
| Předmět: |
|
| Zdroj: |
Neuropsychopharmacology; Jun2006, Vol. 31 Issue 6, p1158-1164, 7p, 1 Color Photograph, 4 Graphs |
| Abstrakt: |
We previously showed that 20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol (M1), a metabolite of protopanaxadiol-type ginseng saponins by intestinal bacteria had axonal extension activity in degenerated neurons, and improved memory disorder and synaptic loss induced by an active fragment of amyloid β, Aβ(25–35). It is unknown how M1 shows these effects in neurons. To clarify the signal transduction mechanism of M1-induced axonal extension, phosphorylated proteins by M1 stimulation were identified because most cellular signal pathways are regulated by phosphorylation/dephosphorylation. The combination of immunoprecipitation and MALDI-TOF-MS revealed that teneurin-2 and mPar3 were specifically phosphorylated by M1 stimulation. Because mPar3 is known as an axonal specifying molecule and to be regulated by phosphatidylinositol 3-kinase (PI3-kinase), the involvement of teneurin-2 and PI3-kinase in the M1 signal was studied. In teneurin-2-deficient cortical neurons, M1-induced axonal extension and PI3-kinase activation were significantly inhibited. In addition, treatment with PI3-kinase inhibitor also reduced M1-induced axonal extension. These results suggest that M1 induces axonal outgrowth through the teneurin-2—PI3-kinase cascade.Neuropsychopharmacology (2006) 31, 1158–1164. doi:10.1038/sj.npp.1300943; published online 2 November 2005 [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
