| First Author | Gelinas JN | Year | 2007 |
| Journal | J Biol Chem | Volume | 282 |
| Issue | 37 | Pages | 27527-35 |
| PubMed ID | 17635924 | Mgi Jnum | J:124932 |
| Mgi Id | MGI:3722966 | Doi | 10.1074/jbc.M701077200 |
| Citation | Gelinas JN, et al. (2007) ERK and mTOR Signaling Couple beta-Adrenergic Receptors to Translation Initiation Machinery to Gate Induction of Protein Synthesis-dependent Long-term Potentiation. J Biol Chem 282(37):27527-27535 |
| abstractText | beta-Adrenergic receptors critically modulate long-lasting synaptic plasticity and long-term memory in the mammalian hippocampus. Persistent long-term potentiation of synaptic strength requires protein synthesis and has been correlated with some forms of hippocampal long-term memory. However, the intracellular processes that initiate protein synthesis downstream of the beta-adrenergic receptor are unidentified. Here we report that activation of beta-adrenergic receptors recruits ERK and mammalian target of rapamycin signaling to facilitate long-term potentiation maintenance at the level of translation initiation. Treatment of mouse hippocampal slices with a beta-adrenergic receptor agonist results in activation of eukaryotic initiation factor 4E and the eukaryotic initiation factor 4E kinase Mnk1, along with inhibition of the translation repressor 4E-BP. This coordinated activation of translation machinery requires concomitant ERK and mammalian target of rapamycin signaling. Taken together, our data identify distinct signaling pathways that converge to regulate beta-adrenergic receptor-dependent protein synthesis during long-term synaptic potentiation in the hippocampus. We suggest that beta-adrenergic receptors play a crucial role in gating the induction of long-lasting synaptic plasticity at the level of translation initiation, a mechanism that may underlie the ability of these receptors to influence the formation of long-lasting memories. |
