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ERIC Number: EJ782523
Record Type: Journal
Publication Date: 2008-Jan
Pages: 7
Abstractor: Author
Reference Count: 0
ISSN: ISSN-1072-0502
Is the Medial Amygdala Part of the Neural Circuit Modulating Conditioned Defeat in Syrian Hamsters?
Markham, Chris M.; Huhman, Kim L.
Learning & Memory, v15 n1 p6-12 Jan 2008
Conditioned defeat is a model wherein hamsters that have previously experienced a single social defeat subsequently exhibit heightened levels of avoidance and submission in response to a smaller, non-aggressive intruder. While we have previously demonstrated the critical involvement of the basolateral and central nuclei of the amygdala in the acquisition and expression of conditioned defeat, the role of the medial amygdala has yet to be investigated. In Experiment 1, muscimol, a GABA[subscript A] receptor agonist, was infused bilaterally into the MeA prior to initial defeat training. Experiment 2 examined the effects of muscimol injections given prior to subsequent testing with a non-aggressive intruder. Finally, in Experiment 3, anisomycin was used to block protein synthesis in the medial and basolateral amygdala to examine the involvement of these nuclei in memory consolidation related to conditioned defeat. Submissive behavior was significantly reduced in animals that received muscimol prior to initial defeat training as well as in animals injected prior to testing with the non-aggressive intruder, indicating that the MeA is necessary for the acquisition and expression of conditioned defeat. In Experiment 3, however, anisomycin reduced conditioned defeat only when administered into the BLA, and not when injected into the MeA. The results of the present series of experiments suggest that, while the MeA may serve an important gateway for sensory information that is crucial for conditioned defeat, it does not appear to play a role in the plasticity including this behavioral response to social defeat.
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Publication Type: Journal Articles; Reports - Research
Education Level: N/A
Audience: N/A
Language: English
Sponsor: N/A
Authoring Institution: N/A