Arc restores juvenile plasticity in adult mouse visual cortex
Name
PNAS-2017-Jenks-9182-7.pdf
Size
1.49 MB
Format
Adobe PDF
Checksum (MD5)
eef31760230b8a351a9b0e7911177d2d
Author(s)
Jenks, Kyle R.
Pastuzyn, Elissa D.
Okuno, Hiroyuki
Taibi, Andrew V.
Bito, Haruhiko
Shepherd, Jason D.
Kim, Taekeun
Bear, Mark
Date Issued
August 2017
Journal
Proceedings of the National Academy of Sciences of the United States of America
Publisher
National Academy of Sciences (U.S.)
Citation
Jenks, Kyle R., Taekeun Kim, Elissa D. Pastuzyn, Hiroyuki Okuno, Andrew V. Taibi, Haruhiko Bito, Mark F. Bear, and Jason D. Shepherd. “Arc Restores Juvenile Plasticity in Adult Mouse Visual Cortex.” Proceedings of the National Academy of Sciences 114, no. 34 (August 8, 2017): 9182–9187. © 2017 National Academy of Sciences
Version
Final published version
Abstract
The molecular basis for the decline in experience-dependent neural plasticity over age remains poorly understood. In visual cortex, the robust plasticity induced in juvenile mice by brief monocular deprivation during the critical period is abrogated by genetic deletion of Arc, an activity-dependent regulator of excitatory synaptic modification. Here, we report that augmenting Arc expression in adult mice prolongs juvenile-like plasticity in visual cortex, as assessed by recordings of ocular dominance (OD) plasticity in vivo. A distinguishing characteristic of juvenile OD plasticity is the weakening of deprived-eye responses, believed to be accounted for by the mechanisms of homosynaptic long-term depression (LTD). Accordingly, we also found increased LTD in visual cortex of adult mice with augmented Arc expression and impaired LTD in visual cortex of juvenile mice that lack Arc or have been treated in vivo with a protein synthesis inhibitor. Further, we found that although activity-dependent expression of Arc mRNA does not change with age, expression of Arc protein is maximal during the critical period and declines in adulthood. Finally, we show that acute augmentation of Arc expression in wild-type adult mouse visual cortex is sufficient to restore juvenile-like plasticity. Together, our findings suggest a unifying molecular explanation for the age- and activity-dependent modulation of synaptic sensitivity to deprivation.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Picower Institute for Learning and Memory
Terms of Use
Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1073/PNAS.1700866114
