期刊
JOURNAL OF NEUROSCIENCE
卷 32, 期 39, 页码 13582-13586出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0809-12.2012
关键词
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L-type voltage-gated calcium channels (L-VGCCs) in the basolateral nucleus of the amygdala (BLA) are necessary for long-term memory of fear conditioning, where they are thought to drive the activation of protein kinases and to initiate gene transcription. However, their role in fear extinction learning is unclear given that systemic injections of VGCC antagonists induce a protracted stress response. Here we tested the effects of local infusions of the L-VGCC antagonists verapamil and nifedipine on both within-session extinction and fear extinction consolidation. Intra-BLA infusions of verapamil or nifedipine did not affect the expression of fear conditioning or the amount of within-session extinction but impaired extinction memory when rats were tested 24 h later drug-free. L-VGCC antagonists also prevented the increase in phosphorylated mitogen-activated protein kinase (MAPK) normally seen in the BLA following extinction learning. These results suggest that activation of L-VGCCs in the BLA at the time of fear extinction learning is necessary for the long-term retention of fear extinction via the MAPK pathway.
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