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The Journal of Neuroscience, June 3, 2009, 29(22):7379-7388; doi:10.1523/JNEUROSCI.0740-09.2009

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Behavioral/Systems/Cognitive
The Central Nucleus of the Amygdala and Corticotropin-Releasing Factor: Insights into Contextual Fear Memory

Matthew W. Pitts,¹ Cedomir Todorovic,² Thomas Blank,² and Lorey K. Takahashi^1,3

¹Department of Cell & Molecular Biology and ²Specialized Neuroscience Research Project 2, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii 96813, and ³Department of Psychology, University of Hawaii, Honolulu, Hawaii 96822

Correspondence should be addressed to Dr. Lorey K. Takahashi, Department of Psychology, University of Hawaii, 2430 Campus Road, Honolulu, HI 96822. Email: LKT{at}hawaii.edu

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.

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Received Feb. 12, 2009; revised April 30, 2009; accepted May 2, 2009.

Correspondence should be addressed to Dr. Lorey K. Takahashi, Department of Psychology, University of Hawaii, 2430 Campus Road, Honolulu, HI 96822. Email: LKT{at}hawaii.edu

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