ArticleLearning & memory (Cold Spring Harbor, N.Y.)2019
Induction of β-adrenergic metaplasticity of LTP requires intact anchoring of PKA.
Article in Learning & memory (Cold Spring Harbor, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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0 citing papers in PubMed, 2 citations in OpenAlex.
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3 authors at 1 institution in 1 country.
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Abstract
Beta-adrenergic receptors (β-ARs) prime hippocampal synapses to stabilize long-term potentiation (LTP). This "metaplasticity" can persist for 1-2 h after pharmacologic activation of β-ARs. It requires activation of PKA (cAMP-dependent protein kinase) during β-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 β-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 β-AR-mediated metaplasticity. These findings implicate PKA anchoring in the induction of β-adrenergic metaplasticity of LTP.
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