Induction of [?eta]-Adrenergic Metaplasticity of LTP Requires Intact Anchoring of PKA

Autor/inn/en	Hoffman, Janlyn R.; Brandwein, Nathan J.; Nguyen, Peter V.
Titel	Induction of [?eta]-Adrenergic Metaplasticity of LTP Requires Intact Anchoring of PKA
Quelle	In: Learning & Memory, 26 (2019) 6, S.187-190 (5 Seiten) PDF als Volltext Verfügbarkeit
Sprache	englisch
Dokumenttyp	gedruckt; online; Zeitschriftenaufsatz
ISSN	1072-0502
DOI	10.1101/lm.049635.119
Schlagwörter	Animals; Science Experiments; Foreign Countries; Stimulation; Logical Thinking; Brain; Memory; Brain Hemisphere Functions; Canada + Suchen Sie Ihr Suchwort? Animal; Tier; Tiere; Ausland; Gehirn; Gedächtnis; Kanada
Abstract	Beta-adrenergic receptors ([beta]-ARs) prime hippocampal synapses to stabilize long-term potentiation (LTP). This "metaplasticity" can persist for 1-2 h after pharmacologic activation of [beta]-ARs. It requires activation of PKA (cAMP-dependent protein kinase) during [beta]-AR priming. A-kinase anchoring proteins (AKAPs) tether PKA to downstream signaling proteins. We hypothesized that induction of this metaplasticity requires intact functioning of AKAPs. Acute application of stearated ht31, a membrane-permeant inhibitor of AKAPs, either during [beta]-AR activation 30 min prior to LTP induction or during LTP induction, attenuated the persistence of LTP. A control, inactive ht31 peptide did not affect [beta]-AR-mediated metaplasticity. These findings implicate PKA anchoring in the induction of [beta]-adrenergic metaplasticity of LTP. (As Provided).
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Erfasst von	ERIC (Education Resources Information Center), Washington, DC
Update	2020/1/01