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J Neurosci. 2012 Feb 8;32(6):1932-41. doi: 10.1523/JNEUROSCI.5231-11.2012.

Redundant catecholamine signaling consolidates fear memory via phospholipase C.

Author information

1
Department of Pharmacology and Neuroscience Graduate Group, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6084, USA.

Abstract

Memories for emotionally arousing experiences are typically vivid and persistent. The recurrent, intrusive memories of traumatic events in post-traumatic stress disorder (PTSD) are an extreme example. Stress-responsive neurotransmitters released during emotional arousal are proposed to enhance the consolidation of fear memory. These transmitters may include norepinephrine and epinephrine (NE/E) because stimulating β-adrenergic receptors shortly after training can enhance memory consolidation. However, mice lacking NE/E acquire and consolidate fear memory normally. Here, we show by using pharmacologic and genetic manipulations in mice and rats that NE/E are not essential for classical fear memory consolidation because signaling by the β(2)-adrenergic receptor is redundant with signaling by dopamine at the D(5)-dopaminergic receptor. The intracellular signaling that is stimulated by these receptors to promote consolidation uses distinct G proteins to redundantly activate phospholipase C. The results support recent evidence indicating that blocking β-adrenergic receptors alone shortly after trauma may not be sufficient to prevent PTSD.

PMID:
22323706
PMCID:
PMC3306178
DOI:
10.1523/JNEUROSCI.5231-11.2012
[Indexed for MEDLINE]
Free PMC Article

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