期刊
FRONTIERS IN BEHAVIORAL NEUROSCIENCE
卷 4, 期 -, 页码 -出版社
FRONTIERS RES FOUND
DOI: 10.3389/neuro.08.002.2010
关键词
amygdala; fear conditioning; auditory thalamus; EGR-1; nitric oxide
资金
- National Science Foundation [NSF 0444632]
- National Institutes of Health [MH 073949]
- New Zealand Tertiary Education Commission
- Yale University
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH073949] Funding Source: NIH RePORTER
In both invertebrate and vertebrate models of synaptic plasticity, signaling via the putative retrograde messenger nitric oxide (NO) has been hypothesized to serve as a critical link between functional and structural alterations at pre- and postsynaptic sites. However, while in vitro models of synaptic plasticity have consistently implicated NO signaling in linking postsynaptic induction mechanisms with accompanying presynaptic changes, a convincing role of such retrograde signaling in mammalian memory formation has remained elusive. Using auditory Pavlovian fear conditioning, we show that synaptic plasticity and NO signaling in the lateral nucleus of the amygdala (LA) regulate the expression of the ERK-driven immediate early gene early growth response gene I (EGR-1) in regions of the auditory thalamus that are presynaptic to the LA. Further, antisense knockdown of EGR-1 in the auditory thalamus impairs both fear memory consolidation and the training-induced elevation of two presynaptically localized proteins in the LA. These findings indicate that synaptic plasticity and NO signaling in the LA during auditory fear conditioning promote alterations in ERK-driven gene expression in auditory thalamic neurons that are required for both fear memory consolidation as well as presynaptic correlates of fear memory formation in the LA, and provide general support for a role of NO as a retrograde signal in mammalian memory formation.
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