title: The immunobiology of sexual behavior: gender differences in the suppression of sexual activity during illness.
abstract: Following infection or injury, sick individuals experience profound psychological and behavioral changes, such as anorexia, depressed activity, and reduced self-care behavior. In the present review, we present evidence for a gender-difference in the behavioral response to sickness. Specifically, following immune activation, sexual activity is suppressed in female, but not in male rats. This gender difference is specific to sexually related responses, because other behaviors, such as locomotion, are equally affected by immune challenges in males and estrous females. The suppression of female sexual behavior, induced by either endotoxin (lipopolysaccharide), or the cytokine interleukin-1 (IL-1), are mediated by central mechanisms that are independent of alterations in ovarian hormone secretion. Furthermore, synergistic effects of the cytokines IL-1 and tumor necrosis factor alpha (TNF alpha) are involved in modulating sexual behavior in sick females, and prostaglandins synthesis is required for the effects of IL-1 on female sexual behavior. The gender difference in the behavioral response to immune activation may be related to the findings that at the same doses and timing in which IL-1 suppressed sexual activity in female but not in male rats, females produced more prostaglandin E2 (PGE2) in the brain, and less corticosterone than males. Finally, we are suggesting that the suppressive effect of cytokines on female reproductive behavior may serve as a mechanism to reduce conception during infection, which exposes the mother and the fetus to dangers such as spontaneous abortions, preterm labor and maternal mortality.
authors.affiliation: Department of Psychology, The Hebrew University of Jerusalem, Mount Scopus, Israel.
authors.forename: R
authors.initials: R
authors.lastname: Avitsur
authors.forename: R
authors.initials: R
authors.lastname: Yirmiya
mesh_terms: D000818:Animals; D012739:Gonadal Steroid Hormones / Q000502:physiology; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism; D009490:Neurosecretory Systems / Q000502:physiology; D011453:Prostaglandins / Q000378:metabolism; D012098:Reproduction / Q000502:physiology*; D012727:Sex Characteristics; D012726:Sexual Behavior, Animal / Q000502:physiology*; D012803:Sick Role; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D012739:Gonadal Steroid Hormones; D007375:Interleukin-1; D011453:Prostaglandins; D014409:Tumor Necrosis Factor-alpha