期刊
JOURNAL OF NEUROSCIENCE
卷 32, 期 6, 页码 1932-1941出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.5231-11.2012
关键词
-
资金
- Department of Defense [PT075099]
- NIH [5R01MH063352]
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 P-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 beta(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 p-adrenergic receptors alone shortly after trauma may not be sufficient to prevent PTSD.
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