Maternal aggression persists following lipopolysaccharide-induced activation of the immune system.

Journal Article (Journal Article)

Lactating females direct aggressive behaviors towards intruders presumably to reduce the likelihood of infanticide of their pups. Infected animals display a constellation of responses that include lethargy, anorexia, and decreased social interactions. This suite of responses is referred to as sickness behavior, and is putatively part of an adaptive strategy to aid the organism in recovery from infection. Previous work has suggested that animals can suppress the behavioral symptoms of sickness in order to engage in adaptive behaviors. To test whether adaptive nest defense is affected by illness, dams received a peripheral injection of either saline or lipopolysaccharide (LPS [50, 400, or 1000 microg/kg]), a non-replicating component of bacterial cell walls that activates the immune system. Simulated infection with LPS reduced body mass and food intake in dams and interfered with litter growth in a dose-dependent manner. Generally, nest defense was unaffected by LPS; the proportion of dams displaying maternal aggression against a male intruder, as well as the latency and duration of aggressive encounters were only suppressed at the highest LPS dose tested. Further, LPS treatment also altered non-agonistic behavior during the aggression test as indicated by reduced social investigation of the intruder and an increased time spent immobile during the session. LPS administration also significantly increased serum corticosterone concentrations in lactating females. These findings suggest that maternal aggression is not suppressed by LPS-evoked immune activation at doses that attenuate other aspects of maternal and social behavior.

Full Text

Duke Authors

Cited Authors

  • Weil, ZM; Bowers, SL; Dow, ER; Nelson, RJ

Published Date

  • April 15, 2006

Published In

Volume / Issue

  • 87 / 4

Start / End Page

  • 694 - 699

PubMed ID

  • 16490223

International Standard Serial Number (ISSN)

  • 0031-9384

Digital Object Identifier (DOI)

  • 10.1016/j.physbeh.2006.01.005

Language

  • eng

Conference Location

  • United States