Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 105, Issue 41, Pages 16015-16020Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0804801105
Keywords
FMRP; GluR1; local protein translation; synaptic scaling
Categories
Funding
- Mabel and Arnold Beckman Foundation
- David and Lucile Packard Foundation
- W. M. Keck Foundation
- National Institutes of Health
Ask authors/readers for more resources
Homeostatic plasticity is thought to play an important role in maintaining the stability of neuronal circuits. During one form of homeostatic plasticity, referred to as synaptic scaling, activity blockade leads to a compensatory increase in synaptic transmission by stimulating in dendrites the local translation and synaptic insertion of the AMPA receptor subunit GluR1. We have previously shown that all-trans retinoic acid (RA) mediates activity blockade-induced synaptic scaling by activating dendritic GluR1 synthesis and that this process requires RAR alpha, a member of the nuclear RA receptor family. This result raised the question of where RAR alpha is localized in dendrites and whether its localization is regulated by RA and/or activity blockade. Here, we show that activity blockade or RA treatment in neurons enhances the concentration of RAR alpha in the dendritic RNA granules and activates local GluR1 synthesis in these RNA granules. Importantly, the same RNA granules that contain RAR alpha also exhibit an accumulation of GluR1 protein but with a much slower time course than that of RARa, suggesting that the former regulates the latter. Taken together, our results provide a direct link between dendritically localized RAR alpha and local GluR1 synthesis in RNA granules during RA-mediated synaptic signaling in homeostatic synaptic plasticity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available