Induction of β-adrenergic metaplasticity of LTP requires intact anchoring of PKA
- Department of Physiology, University of Alberta School of Medicine, Edmonton, Alberta T6G 2H7, Canada
- Corresponding author: peter.nguyen{at}ualberta.ca
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.
Footnotes
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Article is online at http://www.learnmem.org/cgi/doi/10.1101/lm.049635.119.
- Received March 3, 2019.
- Accepted April 23, 2019.
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