PMID- 21746789 OWN - NLM STAT- MEDLINE DCOM- 20160422 LR - 20211020 IS - 1469-7793 (Electronic) IS - 0022-3751 (Print) IS - 0022-3751 (Linking) VI - 589 IP - 17 DP - 2011 Sep 1 TI - Activation of beta-adrenergic receptors facilitates heterosynaptic translation-dependent long-term potentiation. PG - 4321-40 LID - 10.1113/jphysiol.2011.209379 [doi] AB - Noradrenaline critically modulates the ability of synapses to undergo long-term plasticity on time scales extending well beyond fast synaptic transmission. Noradrenergic signalling through beta-adrenergic receptors (beta-ARs) enhances memory consolidation and can boost the longevity of long-term potentiation (LTP). Previous research has shown that stimulation of one synaptic pathway with a protocol that induces persistent, translation-dependent LTP can enable the induction of LTP by subthreshold stimulation at a second, independent synaptic pathway. This heterosynaptic facilitation depends on the regulation and synthesis of proteins. Recordings taken from area CA1 in mouse hippocampal slices showed that induction of beta-AR-dependent LTP at one synaptic pathway (S1) can facilitate LTP at a second, independent pathway (S2) when low-frequency, subthreshold stimulation is applied after a 30 min delay. beta-AR-dependent heterosynaptic facilitation requires protein synthesis as inhibition of mammalian target of rapamycin (mTOR), extracellular signal-regulated kinase (ERK), or translation, prevented homo- and heterosynaptic LTP. Shifting application of a translational repressor, emetine, to coincide with S2 stimulation did not block LTP. Heterosynaptic LTP was prevented in the presence of the cell-permeable cAMP-dependent protein kinase inhibitor, PKI. Conversely, the time window for inter-pathway transfer of heterosynaptic LTP was extended through inhibition of GluR2 endocytosis. Our data show that activation of beta-ARs boosts the heterosynaptic expression of translation-dependent LTP. These results suggest that engagement of the noradrenergic system may extend the associative capacity of hippocampal synapses through facilitation of intersynaptic crosstalk. FAU - Connor, Steven A AU - Connor SA AD - Centre for Neuroscience, University of Alberta School of Medicine, Medical Sciences Building, Edmonton, Canada. FAU - Wang, Yu Tian AU - Wang YT FAU - Nguyen, Peter V AU - Nguyen PV LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20110711 PL - England TA - J Physiol JT - The Journal of physiology JID - 0266262 RN - 0 (Receptors, Adrenergic, beta) SB - IM MH - Animals MH - Electric Stimulation MH - Hippocampus MH - *Long-Term Potentiation MH - Mice, Inbred C57BL MH - *Receptors, Adrenergic, beta PMC - PMC3180585 EDAT- 2011/07/13 06:00 MHDA- 2016/04/23 06:00 PMCR- 2012/09/01 CRDT- 2011/07/13 06:00 PHST- 2011/07/13 06:00 [entrez] PHST- 2011/07/13 06:00 [pubmed] PHST- 2016/04/23 06:00 [medline] PHST- 2012/09/01 00:00 [pmc-release] AID - jphysiol.2011.209379 [pii] AID - 10.1113/jphysiol.2011.209379 [doi] PST - ppublish SO - J Physiol. 2011 Sep 1;589(17):4321-40. doi: 10.1113/jphysiol.2011.209379. Epub 2011 Jul 11.