TY - JOUR T1 - Extracellular Signal-Regulated Kinase 2 (ERK2) Knockdown Mice Show Deficits in Long-Term Memory; ERK2 Has a Specific Function in Learning and Memory JF - The Journal of Neuroscience JO - J. Neurosci. SP - 10765 LP - 10776 DO - 10.1523/JNEUROSCI.0117-07.2007 VL - 27 IS - 40 AU - Yasushi Satoh AU - Shogo Endo AU - Toshio Ikeda AU - Kazuyuki Yamada AU - Masataka Ito AU - Masahiko Kuroki AU - Takeshi Hiramoto AU - Osamu Imamura AU - Yasushi Kobayashi AU - Yasuhiro Watanabe AU - Shigeyoshi Itohara AU - Kunio Takishima Y1 - 2007/10/03 UR - http://www.jneurosci.org/content/27/40/10765.abstract N2 - The extracellular signal-regulated kinase (ERK) 1 and 2 are important signaling components implicated in learning and memory. These isoforms display a high degree of sequence homology and share a similar substrate profile. However, recent findings suggest that these isoforms may have distinct roles: whereas ERK1 seems to be not so important for associative learning, ERK2 might be critically involved in learning and memory. Thus, the individual role of ERK2 has received considerable attention, although it is yet to be understood. Here, we have generated a series of mice in which ERK2 expression decreased in an allele dose-dependent manner. Null ERK2 knock-out mice were embryonic lethal, and the heterozygous mice were anatomically impaired. To gain a better understanding of the influence of ERK2 on learning and memory, we also generated knockdown mice in which ERK2 expression was partially (20–40%) reduced. These mutant mice were viable and fertile with normal appearance. The mutant mice showed a deficit in long-term memory in classical fear conditioning, whereas short-term memory was normal. The mice also showed learning deficit in the water maze and the eight-arm radial maze. The ERK1 expression level of the knockdown mice was comparable with the wild-type control. Together, our results indicate a noncompensable role of ERK2-dependent signal transduction in learning and memory. ER -