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Induction of ?-adrenergic metaplasticity of LTP requires intact anchoring of PKA.

ABSTRACT: Beta-adrenergic receptors (?-ARs) prime hippocampal synapses to stabilize long-term potentiation (LTP). This "metaplasticity" can persist for 1-2 h after pharmacologic activation of ?-ARs. It requires activation of PKA (cAMP-dependent protein kinase) during ?-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 ?-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 ?-AR-mediated metaplasticity. These findings implicate PKA anchoring in the induction of ?-adrenergic metaplasticity of LTP.

SUBMITTER: Hoffman JR 

PROVIDER: S-EPMC6529881 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature

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Induction of β-adrenergic metaplasticity of LTP requires intact anchoring of PKA.

Hoffman Janlyn R JR   Brandwein Nathan J NJ   Nguyen Peter V PV  

Learning & memory (Cold Spring Harbor, N.Y.) 20190520 6

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-permean  ...[more]

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