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| Content Provider | PubMed Central |
|---|---|
| Author | Arendt, Kristin L. Zhang, Zhenjie Ganesan, Subhashree Hintze, Maik Shin, Maggie M. Tang, Yitai Cho, Ahryon Graef, Isabella A. Chen, Lu |
| Abstract | Chronic reduction of synaptic activity in neural networks leads to compensatory changes at both excitatory and inhibitory synapses, a phenomenon known as homeostatic synaptic plasticity. Postsynaptic activity/Ca2+-dependent regulation of retinoic acid (RA) synthesis is critically involved in homeostatic synaptic plasticity; however, the signaling molecule that gates RA synthesis in response to Ca2+ level changes remains unknown. Using pharmacologic and genetic manipulations, we show that calcineurin (CaN) activity, which is regulated by postsynaptic Ca2+ levels, directly controls RA synthesis. Inhibiting CaN activity or genetic ablation of CaN leads to homeostatic modulation of synaptic transmission in an RA signaling-dependent manner. These findings uncover the molecular mechanism by which activity regulates synaptic strength through RA synthesis. |
| Related Links | http://dx.doi.org/10.1073/pnas.1510239112 |
| Starting Page | 5744 |
| File Format | |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 42 |
| Volume Number | 112 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2015-10-20 |
| Access Restriction | Open |
| Rights Holder | National Academy of Sciences |
| Subject Keyword | General Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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