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dc.contributor.authorRaybuck, Jonathan D.
dc.contributor.authorLattal, K. Matthew
dc.contributor.editorTsien, Joe Z.
dc.date.accessioned2012-10-26T20:27:14Z
dc.date.available2012-10-26T20:27:14Z
dc.date.issued2011-01-19en_US
dc.identifier.citationPLoS One. 2011 Jan 19; 6(1):e15982en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid21283812en_US
dc.identifier.doi10.1371/journal.pone.0015982en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/732
dc.description.abstractA key finding in studies of the neurobiology of learning memory is that the amygdala is critically involved in Pavlovian fear conditioning. This is well established in delay-cued and contextual fear conditioning; however, surprisingly little is known of the role of the amygdala in trace conditioning. Trace fear conditioning, in which the CS and US are separated in time by a trace interval, requires the hippocampus and prefrontal cortex. It is possible that recruitment of cortical structures by trace conditioning alters the role of the amygdala compared to delay fear conditioning, where the CS and US overlap. To investigate this, we inactivated the amygdala of male C57BL/6 mice with GABA A agonist muscimol prior to 2-pairing trace or delay fear conditioning. Amygdala inactivation produced deficits in contextual and delay conditioning, but had no effect on trace conditioning. As controls, we demonstrate that dorsal hippocampal inactivation produced deficits in trace and contextual, but not delay fear conditioning. Further, pre- and post-training amygdala inactivation disrupted the contextual but the not cued component of trace conditioning, as did muscimol infusion prior to 1- or 4-pairing trace conditioning. These findings demonstrate that insertion of a temporal gap between the CS and US can generate amygdala-independent fear conditioning. We discuss the implications of this surprising finding for current models of the neural circuitry involved in fear conditioning.
dc.rightsThis is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.en_US
dc.subjectResearch Articleen_US
dc.subjectBiologyen_US
dc.subjectModel Organismsen_US
dc.subjectAnimal Modelsen_US
dc.subjectMouseen_US
dc.subjectNeuroscienceen_US
dc.subjectCognitive Neuroscienceen_US
dc.subjectWorking Memoryen_US
dc.subjectBehavioral Neuroscienceen_US
dc.subjectLearning and Memoryen_US
dc.subjectSocial and Behavioral Sciencesen_US
dc.subjectPsychologyen_US
dc.subjectBehavioren_US
dc.subjectEmotionsen_US
dc.subjectExperimental Psychologyen_US
dc.subjectPsychological Stressen_US
dc.titleDouble Dissociation of Amygdala and Hippocampal Contributions to Trace and Delay Fear Conditioningen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3023765en_US
dc.contributor.corporatenameDepartment of Neurology
refterms.dateFOA2019-04-10T00:41:21Z
html.description.abstractA key finding in studies of the neurobiology of learning memory is that the amygdala is critically involved in Pavlovian fear conditioning. This is well established in delay-cued and contextual fear conditioning; however, surprisingly little is known of the role of the amygdala in trace conditioning. Trace fear conditioning, in which the CS and US are separated in time by a trace interval, requires the hippocampus and prefrontal cortex. It is possible that recruitment of cortical structures by trace conditioning alters the role of the amygdala compared to delay fear conditioning, where the CS and US overlap. To investigate this, we inactivated the amygdala of male C57BL/6 mice with GABA A agonist muscimol prior to 2-pairing trace or delay fear conditioning. Amygdala inactivation produced deficits in contextual and delay conditioning, but had no effect on trace conditioning. As controls, we demonstrate that dorsal hippocampal inactivation produced deficits in trace and contextual, but not delay fear conditioning. Further, pre- and post-training amygdala inactivation disrupted the contextual but the not cued component of trace conditioning, as did muscimol infusion prior to 1- or 4-pairing trace conditioning. These findings demonstrate that insertion of a temporal gap between the CS and US can generate amygdala-independent fear conditioning. We discuss the implications of this surprising finding for current models of the neural circuitry involved in fear conditioning.


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