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dc.contributor.authorOta, Kristie T.
dc.contributor.authorMonsey, Melissa S.
dc.contributor.authorWu, Melissa S.
dc.contributor.authorSchafe, Glenn E.
dc.contributor.editorTsien, Joe Z.
dc.date.accessioned2012-10-26T16:26:48Z
dc.date.available2012-10-26T16:26:48Z
dc.date.issued2010-06-21en_US
dc.identifier.citationPLoS One. 2010 Jun 21; 5(6):e11236en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid20574537en_US
dc.identifier.doi10.1371/journal.pone.0011236en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/588
dc.description.abstractIn vertebrate models of synaptic plasticity, signaling via the putative â retrograde messengerâ nitric oxide (NO) has been hypothesized to serve as a critical link between functional and structural alterations at pre- and postsynaptic sites. In the present study, we show that auditory Pavlovian fear conditioning is associated with significant and long-lasting increases in the expression of the postsynaptically-localized protein GluR1 and the presynaptically-localized proteins synaptophysin and synapsin in the lateral amygdala (LA) within 24 hrs following training. Further, we show that rats given intra-LA infusion of either the NR2B-selective antagonist Ifenprodil, the NOS inhibitor 7-Ni, or the PKG inhibitor Rp-8-Br-PET-cGMPS exhibit significant decreases in training-induced expression of GluR1, synaptophysin, and synapsin immunoreactivity in the LA, while those rats infused with the PKG activator 8-Br-cGMP exhibit a significant increase in these proteins in the LA. In contrast, rats given intra-LA infusion of the NO scavenger c-PTIO exhibit a significant decrease in synapsin and synaptophysin expression in the LA, but no significant impairment in the expression of GluR1. Finally, we show that intra-LA infusions of the ROCK inhibitor Y-27632 or the CaMKII inhibitor KN-93 impair training-induced expression of GluR1, synapsin, and synaptophysin in the LA. These findings suggest that the NO-cGMP-PKG, Rho/ROCK, and CaMKII signaling pathways regulate fear memory consolidation, in part, by promoting both pre- and post-synaptic alterations at LA synapses. They further suggest that synaptic plasticity in the LA during auditory fear conditioning promotes alterations at presynaptic sites via NO-driven â retrograde signalingâ .
dc.rightsOta et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.subjectResearch Articleen_US
dc.subjectNeuroscience/Animal Cognitionen_US
dc.subjectNeuroscience/Behavioral Neuroscienceen_US
dc.subjectNeuroscience/Neuronal Signaling Mechanismsen_US
dc.titleSynaptic Plasticity and NO-cGMP-PKG Signaling Regulate Pre- and Postsynaptic Alterations at Rat Lateral Amygdala Synapses Following Fear Conditioningen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC2888610en_US
dc.contributor.corporatenameDepartment of Neurology
dc.contributor.corporatenameCollege of Graduate Studies
refterms.dateFOA2019-04-09T22:03:45Z
html.description.abstractIn vertebrate models of synaptic plasticity, signaling via the putative â retrograde messengerâ nitric oxide (NO) has been hypothesized to serve as a critical link between functional and structural alterations at pre- and postsynaptic sites. In the present study, we show that auditory Pavlovian fear conditioning is associated with significant and long-lasting increases in the expression of the postsynaptically-localized protein GluR1 and the presynaptically-localized proteins synaptophysin and synapsin in the lateral amygdala (LA) within 24 hrs following training. Further, we show that rats given intra-LA infusion of either the NR2B-selective antagonist Ifenprodil, the NOS inhibitor 7-Ni, or the PKG inhibitor Rp-8-Br-PET-cGMPS exhibit significant decreases in training-induced expression of GluR1, synaptophysin, and synapsin immunoreactivity in the LA, while those rats infused with the PKG activator 8-Br-cGMP exhibit a significant increase in these proteins in the LA. In contrast, rats given intra-LA infusion of the NO scavenger c-PTIO exhibit a significant decrease in synapsin and synaptophysin expression in the LA, but no significant impairment in the expression of GluR1. Finally, we show that intra-LA infusions of the ROCK inhibitor Y-27632 or the CaMKII inhibitor KN-93 impair training-induced expression of GluR1, synapsin, and synaptophysin in the LA. These findings suggest that the NO-cGMP-PKG, Rho/ROCK, and CaMKII signaling pathways regulate fear memory consolidation, in part, by promoting both pre- and post-synaptic alterations at LA synapses. They further suggest that synaptic plasticity in the LA during auditory fear conditioning promotes alterations at presynaptic sites via NO-driven â retrograde signalingâ .


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