Dissociable roles of prelimbic and infralimbic cortices, ventral hippocampus, and basolateral amygdala in the expression and extinction of conditioned fear.

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TitleDissociable roles of prelimbic and infralimbic cortices, ventral hippocampus, and basolateral amygdala in the expression and extinction of conditioned fear.
Publication TypeJournal Article
Year of Publication2011
AuthorsSierra-Mercado, D, Padilla-Coreano, N, Quirk, GJ
JournalNeuropsychopharmacology
Volume36
Issue2
Pagination529-38
Date Published2011 Jan
ISSN1740-634X
KeywordsAmygdala, Animals, CA1 Region, Hippocampal, Conditioning, Operant, Extinction, Psychological, Fear, Male, Prefrontal Cortex, Rats, Rats, Sprague-Dawley
Abstract

Current models of conditioned fear expression and extinction involve the basolateral amygdala (BLA), ventral medial prefrontal cortex (vmPFC), and the hippocampus (HPC). There is some disagreement with respect to the specific roles of these structures, perhaps due to subregional differences within each area. For example, growing evidence suggests that infralimbic (IL) and prelimbic (PL) subregions of vmPFC have opposite influences on fear expression. Moreover, it is the ventral HPC (vHPC), rather than the dorsal HPC, that projects to vmPFC and BLA. To help determine regional specificity, we used small doses of the GABA(A) agonist muscimol to selectively inactivate IL, PL, BLA, or vHPC in an auditory fear conditioning and extinction paradigm. Infusions were performed prior to extinction training, allowing us to assess the effects on both fear expression and subsequent extinction memory. Inactivation of IL had no effect on fear expression, but impaired the within-session acquisition of extinction as well as extinction memory. In contrast, inactivation of PL impaired fear expression, but had no effect on extinction memory. Inactivation of the BLA or vHPC impaired both fear expression and extinction memory. Post-extinction inactivations had no effect in any structure. We suggest a model in which amygdala-dependent fear expression is modulated by inputs from PL and vHPC, whereas extinction memory requires extinction-induced plasticity in IL, BLA, and/or vHPC.

DOI10.1038/npp.2010.184
Alternate JournalNeuropsychopharmacology
PubMed ID20962768
PubMed Central IDPMC3005957
Grant ListMH058883 / MH / NIMH NIH HHS / United States
MH081975 / MH / NIMH NIH HHS / United States
R01 MH058883 / MH / NIMH NIH HHS / United States
R01 MH058883-14 / MH / NIMH NIH HHS / United States
R01 MH081975 / MH / NIMH NIH HHS / United States
R01 MH081975-03 / MH / NIMH NIH HHS / United States
R36 MH089296 / MH / NIMH NIH HHS / United States
R36 MH089296-01 / MH / NIMH NIH HHS / United States
T34 GM007821 / GM / NIGMS NIH HHS / United States