| First Author | Arai JA | Year | 2009 |
| Journal | Neurosci Lett | Volume | 455 |
| Issue | 1 | Pages | 22-5 |
| PubMed ID | 19429099 | Mgi Jnum | J:150447 |
| Mgi Id | MGI:3850785 | Doi | 10.1016/j.neulet.2009.03.047 |
| Citation | Arai JA, et al. (2009) Sos2 is dispensable for NMDA-induced Erk activation and LTP induction. Neurosci Lett 455(1):22-5 |
| abstractText | N-methyl-d-aspartate (NMDA) receptor-induced activation of extracellular signal-related protein kinase (Erk) plays important roles in various neuronal functions including long-term potentiation (LTP). Son of sevenless (Sos) proteins have been implicated in NMDA-induced Erk activation in neurons of young mice. However, contribution of each of the two Sos isoforms, Sos1 and Sos2, has not been clarified. In this study, Sos2 involvement in NMDA-induced Erk activation was examined. We observed no defect in Erk phosphorylation induced by NMDA treatment of cortical neuronal cultures from Sos2-/- newborn mice. Moreover, theta-burst-induced LTP induction in the hippocampus of Sos2-/- mice was also normal. Finally, Erk activation by either depolarization or BDNF treatment was also normal in cultured neurons from Sos2 knockout mice. These results imply that Sos1 is the major regulator of these well-known neuronal Sos functions and suggest that a novel function for Sos2 in neurons remains to be determined. |
