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Brain Res Bull. 2018 Jul;141:50-57. doi: 10.1016/j.brainresbull.2018.04.011. Epub 2018 Apr 20.

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

Author information

1
Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 08826, South Korea; Department of Pharmacology, Wonkwang University School of Medicine, Iksan 54538, South Korea.
2
School of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan 44919, South Korea.
3
Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 08826, South Korea.
4
Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 08826, South Korea. Electronic address: kaang@snu.ac.kr.

Abstract

Memory reconsolidation is the process by which previously consolidated memories reenter a labile state through reactivation of the memory trace and are actively consolidated through de novo protein synthesis. Although extensive studies have shown that β-adrenergic signaling plays a critical role in the restabilization of reactivated memory, its role in the destabilization of long-term memory is not well-studied. 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.

KEYWORDS:

Long-term memory; Membrane excitability; Propranolol; Reconsolidation; β-adrenergic signaling

[Indexed for MEDLINE]

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