β-Adrenergic signaling is required for the induction of a labile state during memory reconsolidation.

In this study, we found that membrane excitability increased in hippocampal CA1 neurons immediately after the retrieval of contextual fear memory. Interestingly, this increase in membrane excitability diminished after treatment with propranolol (a β-adrenergic receptor antagonist), an NMDA receptor antagonist, and a PKA inhibitor. In addition, we found that administration of propranolol prior to, but not after, the retrieval of fear memory ameliorated the memory impairment caused by anisomycin, indicating that inhibition of β-adrenergic signaling blocks the destabilization of contextual fear memory. Taken together, these results indicate that β-adrenergic signaling via NMDA receptors and PKA signaling pathway induces a labile state of long-term memory through increased neuronal membrane excitability.
PMID: 29680772 [PubMed - as supplied by publisher]

Source: Brain Research Bulletin - April 19, 2018 Category: Neurology Authors: Lim CS, Kim JI, Kwak C, Lee J, Jang EH, Oh J, Kaang BK Tags: Brain Res Bull Source Type: research