Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, United States
Wade Morishita
Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, United States
Salvatore Incontro
Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, United States
Jeffrey Simms
Gladstone Institute of Neurological Disease, San Francisco, United States
Julia Holtzman
Gladstone Institute of Neurological Disease, San Francisco, United States
Michael Gill
Gladstone Institute of Neurological Disease, San Francisco, United States
Lennart Mucke
Gladstone Institute of Neurological Disease, San Francisco, United States; Department of Neurology, University of California, San Francisco, San Francisco, United States
Robert C Malenka
Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, United States
We tested the proposal that the C-terminal domain (CTD) of the AMPAR subunit GluA1 is required for LTP. We found that a knock-in mouse lacking the CTD of GluA1 expresses normal LTP and spatial memory, assayed by the Morris water maze. Our results support a model in which LTP generates synaptic slots, which capture passively diffusing AMPARs.
