The regulated trafficking of GluR1 contributes significantly to synaptic plasticity, but studies addressing the function of the GluR1 C-terminal PDZ-Iigand domain in this process have produced conflicting results. Here, we resolve this conflict by showing that apparently similar C-terminal mutations of the GluR1 PDZ-ligand domain result in opposite physiological phenotypes during activity- and CamKII-induced synaptic plasticity.
机构:
Korea Adv Inst Sci & Technol, Natl Creat Res Initiat Ctr Synaptogenesis, Taejon 305701, South KoreaKorea Adv Inst Sci & Technol, Natl Creat Res Initiat Ctr Synaptogenesis, Taejon 305701, South Korea
Kim, EJ
;
Sheng, M
论文数: 0引用数: 0
h-index: 0
机构:Korea Adv Inst Sci & Technol, Natl Creat Res Initiat Ctr Synaptogenesis, Taejon 305701, South Korea
机构:
Korea Adv Inst Sci & Technol, Natl Creat Res Initiat Ctr Synaptogenesis, Taejon 305701, South KoreaKorea Adv Inst Sci & Technol, Natl Creat Res Initiat Ctr Synaptogenesis, Taejon 305701, South Korea
Kim, EJ
;
Sheng, M
论文数: 0引用数: 0
h-index: 0
机构:Korea Adv Inst Sci & Technol, Natl Creat Res Initiat Ctr Synaptogenesis, Taejon 305701, South Korea