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ERIC Number: EJ874489
Record Type: Journal
Publication Date: 2010-Feb
Pages: 11
Abstractor: As Provided
Reference Count: 0
ISBN: N/A
ISSN: ISSN-1072-0502
Role of the Basolateral Amygdala in the Reinstatement and Extinction of Fear Responses to a Previously Extinguished Conditioned Stimulus
Laurent, Vincent; Westbrook, R. Frederick
Learning & Memory, v17 n2 p86-96 Feb 2010
Four experiments used rats to study the role of the basolateral amygdala (BLA) in the reinstatement and extinction of fear responses (freezing) to a previously extinguished conditioned stimulus (CS). In Experiment 1, BLA inactivation before pairing the extinguished CS with the shock unconditioned stimulus (US) or before US-alone exposure impaired the restoration and the reinstatement of fear responses to the extinguished CS. In Experiment 2, BLA inactivation before extinction impaired long-term inhibition of fear responses, but its inactivation before extinction of fear responses restored by CS-US pairing did not impair long-term inhibition. In Experiment 3, BLA inactivation before extinction of fear responses or before the extinction of fear responses reinstated by US-alone exposure impaired long-term inhibition. In Experiment 4, BLA inactivation did not impair long-term inhibition of fear responses reinstated by US-alone exposure if the context where the US-alone exposure occurred had been previously extinguished. These results confirm that the BLA is critical for both learning fear and fear inhibition, but not for relearning this inhibition. The results are consistent with the view that reinstatement is due to the extinguished CS being tested in a dangerous context and are discussed in terms of a contemporary neural model of fear inhibition.
Cold Spring Harbor Laboratory Press. 500 Sunnyside Boulevard, Woodbury, NY 11797-2924. Tel: 800-843-4388; Tel: 516-367-8800; Fax: 516-422-4097; e-mail: cshpres@cshl.edu; Web site: http://www.learnmem.org/
Publication Type: Journal Articles; Reports - Research
Education Level: N/A
Audience: N/A
Language: English
Sponsor: N/A
Authoring Institution: N/A