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Double Dissociation of Amygdala and Hippocampal Contributions to Trace and Delay Fear Conditioning
- Hdl Handle:
- http://hdl.handle.net/10675.2/732
- Title:
- Double Dissociation of Amygdala and Hippocampal Contributions to Trace and Delay Fear Conditioning
- Authors:
- Abstract:
- A 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.
- Editors:
- Tsien, Joe Z.
- Citation:
- PLoS One. 2011 Jan 19; 6(1):e15982
- Issue Date:
- 19-Jan-2011
- URI:
- http://hdl.handle.net/10675.2/732
- DOI:
- 10.1371/journal.pone.0015982
- PubMed ID:
- 21283812
- PubMed Central ID:
- PMC3023765
- Type:
- Article
- ISSN:
- 1932-6203
- Appears in Collections:
- Department of Neurology: Faculty Research and Presentations
Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Raybuck, Jonathan D. | en_US |
dc.contributor.author | Lattal, K. Matthew | en_US |
dc.contributor.editor | Tsien, Joe Z. | - |
dc.date.accessioned | 2012-10-26T20:27:14Z | - |
dc.date.available | 2012-10-26T20:27:14Z | - |
dc.date.issued | 2011-01-19 | en_US |
dc.identifier.citation | PLoS One. 2011 Jan 19; 6(1):e15982 | en_US |
dc.identifier.issn | 1932-6203 | en_US |
dc.identifier.pmid | 21283812 | en_US |
dc.identifier.doi | 10.1371/journal.pone.0015982 | en_US |
dc.identifier.uri | http://hdl.handle.net/10675.2/732 | - |
dc.description.abstract | A 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. | en_US |
dc.rights | This 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.subject | Research Article | en_US |
dc.subject | Biology | en_US |
dc.subject | Model Organisms | en_US |
dc.subject | Animal Models | en_US |
dc.subject | Mouse | en_US |
dc.subject | Neuroscience | en_US |
dc.subject | Cognitive Neuroscience | en_US |
dc.subject | Working Memory | en_US |
dc.subject | Behavioral Neuroscience | en_US |
dc.subject | Learning and Memory | en_US |
dc.subject | Social and Behavioral Sciences | en_US |
dc.subject | Psychology | en_US |
dc.subject | Behavior | en_US |
dc.subject | Emotions | en_US |
dc.subject | Experimental Psychology | en_US |
dc.subject | Psychological Stress | en_US |
dc.title | Double Dissociation of Amygdala and Hippocampal Contributions to Trace and Delay Fear Conditioning | en_US |
dc.type | Article | en_US |
dc.identifier.pmcid | PMC3023765 | en_US |
dc.contributor.corporatename | Department of Neurology | - |
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