Journal
JOURNAL OF NEUROSCIENCE
Volume 31, Issue 19, Pages 7073-7082Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1120-11.2011
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Funding
- National Institutes of Health [MH 073949]
- Yale University
- Department of Defense, Air Force Office of Scientific Research [32 CRF 168a]
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The activity-regulated cytoskeletal-associated protein (Arc/Arg3.1) is an immediate-early gene that has been widely implicated in synaptic plasticity and in the consolidation of a variety of hippocampal-and amygdala-dependent memory tasks. The functional role of Arc/Arg3.1 in memory reconsolidation processes, however, has not been systematically studied. In the present study, we examined the role of Arc/Arg3.1 in the reconsolidation of an amygdala-dependent auditory pavlovian fear memory. We show that Arc/Arg3.1 protein is regulated in the lateral nucleus of the amygdala (LA) by retrieval of an auditory fear memory. Next, we show that antisense knockdown of Arc/Arg3.1 in the LA impairs fear memory reconsolidation of both a recent (1-d-old) as well as a well-consolidated (2-week-old) fear memory; that is, post-retrieval short-term memory, tested at 3 h after retrieval, is intact, whereas post-retrieval long-term memory, tested similar to 24 h after retrieval, is significantly impaired. The effect of Arc/Arg3.1 knockdown was observed to be time limited and specific to an actively reactivated fear memory. Moreover, the reconsolidation deficit induced by Arc/Arg3.1 knockdown was not found to be sensitive to spontaneous recovery, reinstatement, or a shift in the testing context, suggesting that our behavioral effects are not attributable to facilitated extinction. Collectively, our findings provide the first comprehensive look at the functional role of Arc/Arg3.1 in memory reconsolidation processes in the mammalian brain.
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