• Neuroscience · Jan 2004

    Comparative Study

    N-methyl-D-aspartate receptors in the amygdala are necessary for the acquisition and expression of conditioned defeat.

    • A M Jasnow, M A Cooper, and K L Huhman.
    • Center for Behavioral Neuroscience, Department of Psychology, 33 Gilmer Street, Georgia State University, 30303-3082, Atlanta GA, USA.
    • Neuroscience. 2004 Jan 1; 123 (3): 625-34.

    AbstractHere, we describe a biologically relevant model called conditioned defeat that is used to examine behavioral responses to social defeat in Syrian hamsters. In this model experimental animals that are normally aggressive experience social defeat and consequently display high levels of submissive/defensive behavior even in response to non-threatening conspecifics. N-methyl-D-aspartate (NMDA) receptors within the amygdala play an important role in conditioned fear; therefore, the purpose of this study was to examine whether NMDA receptors within the amygdala are necessary for the acquisition and expression of conditioned defeat. Specifically, the present study examined whether bilateral infusions of the NMDA receptor antagonist DL-2-amino-5-phosphonopentanoic acid (AP5; 0.625, 1.25, 2.5, 5.0, 10.0 microg) into the amygdala would block the acquisition of conditioned defeat. Subsequently, we examined whether bilateral infusions of AP5 (0.625, 1.25, 2.5, 5.0 microg) into the amygdala prior to testing would block the expression of conditioned defeat. Infusions of AP5 into the amygdala immediately before the initial social defeat significantly reduced submissive/defensive behavior when hamsters were tested the following day with a non-aggressive intruder. Similarly, infusions of AP5 into the amygdala immediately before exposure to a non-aggressive intruder significantly attenuated the display of submissive/defensive behavior. These data demonstrate that NMDA receptors are necessary for both the acquisition and expression of conditioned defeat. We believe that conditioned defeat is a unique and valuable animal model with which to investigate the neurobiology of fear-related changes in social behavior.

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