XXXX goes nuclear: Epigenetic modifications during long-lasting synaptic potentiation triggered by activation of beta-adrenergic receptors.

@entity1 @entity4778 @entity1063 @entity19
UNASSIGNED: @entity1063 (NE) is a neuromodulator that can effect long-lasting changes in synaptic strength such as long-term potentiation (LTP), a putative cellular mechanism for memory formation in the @entity1 brain. Persistent LTP requires alterations in gene expression that may involve epigenetic mechanisms such as DNA methylation, histone acetylation, and histone phosphorylation. It is known that beta-adrenergic receptors and NE can boost LTP maintenance by regulating translation. However, it is unclear whether NE can additionally engage epigenetic mechanisms to regulate transcription and boost LTP endurance. To address this issue, we probed NE-treated @entity19 hippocampal slices with pharmacological inhibitors targeting epigenetic regulatory pathways and discovered that NE activates beta-adrenergic receptors to boost LTP maintenance in area @entity4778 through DNA methylation and post-translational histone modifications. Specifically, NE paired with 100-Hz stimulation enhanced histone H3 acetylation and phosphorylation, both of which were required for NE-induced boosting of LTP maintenance. Together, our findings identify NE as a neuromodulatory transmitter capable of triggering epigenetic, transcriptional control of genes required for establishing persistent LTP in the @entity19 hippocampus. These modifications may contribute to the stabilization of memory. This article is protected by copyright. All rights reserved.
