Testosterone treatment diminishes sickness behavior in male songbirds.
Males of many vertebrate species are typically more prone to disease and infection than female conspecifics, and this sexual difference is partially influenced by the immunosuppressive properties of testosterone (T) in males. T-induced immunosuppression has traditionally been viewed as a pleiotropic handicap, rather than an adaptation. Recently, it has been hypothesized that suppression of sickness behavior, or the symptoms of infection, may have adaptive value if sickness interferes with the expression of T-mediated behaviors important for male reproductive success. We conduct a classic hormone replacement experiment to examine if T suppresses sickness behavior in a seasonally-breeding songbird, Gambel's white-crowned sparrow (Zonotrichia leucophrys gambelii). Triggered experimentally by bacterial lipopolysaccharide (LPS), sickness behavior includes decreased activity, anorexia, and weight loss. Gonadectomized (GDX) males that were treated with silastic implants filled with T exhibited suppression of behavioral and physiological responses to LPS compared to GDX and sham-GDX controls given empty implants. Sickness responses of control groups were statistically indistinguishable. T-implanted birds had significantly higher plasma T than control groups and levels were within the range associated with aggressive interactions during male-to-male contests. These findings imply that suppression of sickness behavior could occur when T is elevated to socially-modulated levels. Alternatively, it is possible that this suppressive effect is mediated through a stress-induced mechanism, as corticosterone levels were elevated in T-implanted subjects compared to controls. We propose that males wounded and infected during contests may gain a brief selective advantage by suppressing sickness responses that would otherwise impair competitive performance. The cost of immunosuppression would be manifested in males through an increased susceptibility to disease, which is presumably offset by capitalizing upon limited reproductive opportunities.
Department of Biology, University of Washington, Seattle, WA 98195-1800, USA. apnta@uaa.alaska.edu
Noah T
NT
Ashley
Quentin R
QR
Hays
George E
GE
Bentley
John C
JC
Wingfield
D000704:Analysis of Variance; D000728:Androgens / Q000008:administration & dosage* / Q000097:blood; D000818:Animals; D000855:Anorexia / Q000188:drug therapy; D001835:Body Weight / Q000187:drug effects; D004435:Eating / Q000187:drug effects; D020249:Hormone Replacement Therapy; D055809:Illness Behavior / Q000187:drug effects*; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D009043:Motor Activity / Q000187:drug effects; D009919:Orchiectomy; D011863:Radioimmunoassay; D046370:Sparrows; D013739:Testosterone / Q000008:administration & dosage* / Q000097:blood
D000728:Androgens; D008070:Lipopolysaccharides; D013739:Testosterone