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Effects of peripheral immune activation on social behavior and adrenocortical activity in aggressive mice: Genotype‐environment interactions
Author(s) -
Grange Douglas A.,
Hood Kathryn E.,
Ikeda Sandra C.,
Reed Cheryl L.,
Jones Byron C.,
Block Michelle L.
Publication year - 1997
Publication title -
aggressive behavior
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.223
H-Index - 92
eISSN - 1098-2337
pISSN - 0096-140X
DOI - 10.1002/(sici)1098-2337(1997)23:2<93::aid-ab2>3.0.co;2-u
Subject(s) - immune system , corticosterone , aggression , endocrinology , medicine , psychology , spleen , hypothalamus , agonistic behaviour , hormone , developmental psychology , immunology
To explore genetic‐developmental differences in the biobehavioral effects of induced illness, males from two lines of mice selectively bred for high or low levels of aggressive behavior were injected with endotoxin ( Escherichia coli , LPS: 0.25 mg/kg, 1.25 mg/kg, or 2.5 mg, i.p.) or saline. Body temperature, weight, and locomotor activity were monitored immediately before and 8 and 24 hr after injection. Twenty‐four hours after injection, social behaviors were assessed in a 10‐min dyadic test, and hypothalamus, spleen, and serum were collected. In both lines, endotoxin treatment increased behavioral immobility ("freezing") and decreased social exploration. Other effects showed line differences: Males from the high‐aggressive line had a lower threshold to endotoxin‐induced effects on body temperature, weight loss, spleen weight, and corticosterone. Social reactivity (startle response to mild social investigation) increased in the high‐aggressive line and decreased in the low‐aggressive line after treatment. In the high‐aggressive line only, endotoxin decreased attack frequency and increased latency to attack. The interactions between selected line (genotype) and endotoxin treatment (environment) demonstrate that genetic‐developmental differences in social and aggressive behavior may indicate the extent to which immune stimuli (e.g., bacteria, viruses, cytokines) function as "biobehavioral stressors." Aggr. Behav. 23:93–105, 1997.© 1997 Wiley‐Liss, Inc.