RT Journal Article
SR Electronic
T1 The Role of GluA1 in Ocular Dominance Plasticity in the Mouse Visual Cortex
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 15220
OP 15225
DO 10.1523/JNEUROSCI.2078-13.2013
VO 33
IS 38
A1 Ranson, Adam
A1 Sengpiel, Frank
A1 Fox, Kevin
YR 2013
UL http://www.jneurosci.org/content/33/38/15220.abstract
AB Ocular dominance plasticity is a widely studied model of experience-dependent cortical plasticity. It has been shown that potentiation of open eye responses resulting from monocular deprivation relies on a homeostatic response to loss of input from the closed eye, but the mechanisms by which this occurs are not fully understood. The role of GluA1 in the homeostatic component of ocular dominance (OD) plasticity has not so far been tested. In this study, we tested the idea that the GluA1 subunit of the AMPA receptor is necessary for open eye potentiation. We found that open eye potentiation did not occur in GluA1 knock-out (GluA1−/−) mice but did occur in wild-type littermates when monocular deprivation was imposed during the critical period. We also found that depression of the closed eye response that normally occurs in the monocular as well as binocular zone is delayed, but only in the monocular zone in GluA1−/− mice and only in a background strain we have previously shown lacks synaptic scaling (C57BL/6OlaHsd). In adult mice, we found that OD plasticity and facilitation of OD plasticity by prior monocular experience were both present in GluA1−/− mice, suggesting that the GluA1-dependent mechanisms only operate during the critical period.