| First Author | Saviuk N | Year | 2022 |
| Journal | Cell Rep | Volume | 39 |
| Issue | 10 | Pages | 110911 |
| PubMed ID | 35675781 | Mgi Jnum | J:326145 |
| Mgi Id | MGI:7294015 | Doi | 10.1016/j.celrep.2022.110911 |
| Citation | Saviuk N, et al. (2022) Loss of 4E-BP converts cerebellar long-term depression to long-term potentiation. Cell Rep 39(10):110911 |
| abstractText | Genetic perturbances in translational regulation result in defects in cerebellar motor learning; however, little is known about the role of translational mechanisms in the regulation of cerebellar plasticity. We show that genetic removal of 4E-BP, a translational suppressor and target of mammalian target of rapamycin complex 1, results in a striking change in cerebellar synaptic plasticity. We find that cerebellar long-term depression (LTD) at parallel fiber-Purkinje cell synapses is converted to long-term potentiation in 4E-BP knockout mice. Biochemical and pharmacological experiments suggest that increased phosphatase activity largely accounts for the defects in LTD. Our results point to a model in which translational regulation through the action of 4E-BP plays a critical role in establishing the appropriate kinase/phosphatase balance required for normal synaptic plasticity in the cerebellum. |
