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Escalated aggression as a reward: corticosterone and GABAA receptor positive modulators in mice

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Abstract

Rationale

Individuals seek out the opportunity to fight, but the mechanisms behind this positively reinforcing effect of aggression have yet to be understood.

Objectives

The aims of this study were to (1) describe behavioral and corticosterone elevations that occur in aggressive mice conditioned to respond for the opportunity to fight another mouse, (2) determine if corticosterone elevations are necessary for operant responding and escalated aggression, and (3) determine if corticosterone elevations alter the aggression-heightening effects of γ-aminobutyric acid (GABA)A receptor positive modulators.

Methods and results

Aggressive male CFW mice were conditioned to respond under the control of a fixed-interval 10-min (FI10) schedule that reinforced their operant behavior by the presentation of an intruder mouse into their home cage. After the FI10, aggressive behavior was ca. 75% higher than the species-typical levels of fighting and plasma corticosterone was more than twice as high after briefly fighting and/or responding on the FI10 schedule. Inhibition of corticosterone synthesis by metyrapone (30–100 mg/kg) reduced both conditioned responding as well as the aggressive behavior after the FI. Although the benzodiazepine midazolam (0.3–3 mg/kg) heightened species-typical aggressive behavior, it did not increase the high level of aggression engendered by the FI schedule. However, midazolam (0.3 mg/kg) and the neurosteroid allopregnanolone (17 mg/kg) both heightened aggression when given after corticosterone synthesis inhibition by metyrapone (56 mg/kg).

Conclusions

These data suggest that corticosterone elevations are required for responding that is motivated by aggressive behavior and for escalated aggression that follows this responding. Corticosterone elevations also appear to inhibit the aggression heightening effect of GABAA receptor positive modulators.

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Acknowledgements

The research was supported by USPHS research grant AA05122 and grants from the Alcoholic Beverage Medical Research Foundation. E.W.F. is currently supported by a Canadian Institutes of Health Research postdoctoral fellowship. The authors extend their appreciation to J. Thomas Sopko and Dr. Ella Nikulina for their technical assistance, to Sara Faccidomo for helping to prepare the manuscript, and to Drs. Robert Cook and Steven C. Heinrichs for comments on an earlier version.

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  1. Eric W. Fish

    Present address: Department of Neuroscience, Douglas Hospital Research Centre, McGill University, Montreal, Quebec, Canada

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  1. Department of Psychology, Tufts University, Medford, MA, USA

    Eric W. Fish, Joseph F. DeBold & Klaus A. Miczek

  2. Departments of Psychiatry, Pharmacology, and Neuroscience, Tufts University, Boston, MA, USA

    Klaus A. Miczek

  3. Department of Neuroscience, Douglas Hospital Research Centre, 6875 Blvd LaSalle, Montreal, Quebec, H4H 1R3, Canada

    Eric W. Fish

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Fish, E.W., DeBold, J.F. & Miczek, K.A. Escalated aggression as a reward: corticosterone and GABAA receptor positive modulators in mice. Psychopharmacology 182, 116–127 (2005). https://doi.org/10.1007/s00213-005-0064-x

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