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Research article summary (published Jun 2009):

The central nucleus of the amygdala and corticotropin-releasing factor: insights into contextual fear memory.

Full Abstract

The central nucleus of the amygdala (CeA) has been traditionally viewed in fear conditioning to serve as an output neural center that transfers conditioned information formed in the basolateral amygdala to brain structures that generate emotional responses. Recent studies suggest that the CeA may also be involved in fear memory consolidation. In addition, corticotropin-releasing factor systems were shown to facilitate memory consolidation in the amygdala, which contains a high density of CRF immunoreactive cell bodies and fibers in the lateral part of the CeA (CeAl). However, the involvement of CeA CRF in contextual fear conditioning remains poorly understood. Therefore, we first conducted a series of studies using fiber-sparing lesion and reversible inactivation methods to assess the general role of the CeA in contextual fear. We then used identical training and testing procedures to compare and evaluate the specific function of CeA CRF using CRF antisense oligonucleotides (CRF ASO). Rats microinjected with ibotenic acid, muscimol, or a CRF ASO into the CeA before contextual fear conditioning showed typical levels of freezing during acquisition training but exhibited significant reductions in contextual freezing in a retention test 48 h later. Furthermore, CeA inactivation induced by either muscimol or CRF ASO administration immediately before retention testing did not impair freezing, suggesting that the previously observed retention deficits were caused by inhibition of consolidation rather than fear expression. Collectively, our results suggest CeA involvement in the consolidation of contextual fear memory and specifically implicate CeA CRF as an important mediator.

 

Author information

Author/s: Pitts, Matthew W (MW); Todorovic, Cedomir (C); Blank, Thomas (T); Takahashi, Lorey K (LK);

Affiliation: Department of Cell & Molecular Biology, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii 96813, USA.

Grants: NS39406 (Agency:NINDS NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, N.I.H., Extramural

Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience (J Neurosci), published in United States. (Language: eng)

Reference: 2009-Jun; vol 29 (issue 22) : pp 7379-88

Dates: Created 2009/06/04; Completed 2009/06/22; Revised 2009/11/03;

PMID: 19494159, status: MEDLINE (last retrieval date: 11/4/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Associated Chemicals: Excitatory Amino Acid Agonists (0) ; GABA Agonists (0) ; Oligodeoxyribonucleotides, Antisense (0) ; Ibotenic Acid (2552-55-8) ; Muscimol (2763-96-4) ; Corticotropin-Releasing Hormone (9015-71-8) ; Phosphopyruvate Hydratase (EC 4.2.1.11)

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