The immunobiology of sexual behavior: Gender differences in the suppression of sexual activity during illness

被引:81
作者
Avitsur, R [1 ]
Yirmiya, R [1 ]
机构
[1] Hebrew Univ Jerusalem, Dept Psychol, IL-91905 Jerusalem, Israel
关键词
sickness behavior; sexual behavior; cytokines; interleukine-1; tumor necrosis factor-alpha; lipopolysaccharide; brain; rats;
D O I
10.1016/S0091-3057(99)00165-3
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
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 E-2 (PGE(2)) 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. (C) 1999 Elsevier Science Inc.
引用
收藏
页码:787 / 796
页数:10
相关论文
共 118 条
[71]   INTERLEUKIN-1-BETA AND INTERLEUKIN-6 SPECIFICALLY INCREASE THE RELEASE OF PROSTAGLANDIN-E(2) FROM RAT HYPOTHALAMIC EXPLANTS INVITRO [J].
NAVARRA, P ;
POZZOLI, G ;
BRUNETTI, L ;
RAGAZZONI, E ;
BESSER, M ;
GROSSMAN, A .
NEUROENDOCRINOLOGY, 1992, 56 (01) :61-68
[72]   ROLE OF PROSTAGLANDINS IN THE BEHAVIORAL-CHANGES INDUCED BY MURINE INTERLEUKIN-1-ALPHA IN THE RAT [J].
OTTERNESS, IG ;
GOLDEN, HW ;
SEYMOUR, PA ;
ESKRA, JD ;
DAUMY, GO .
CYTOKINE, 1991, 3 (04) :333-338
[73]   THE EFFECTS OF CONTINUOUS ADMINISTRATION OF MURINE INTERLEUKIN-1-ALPHA IN THE RAT [J].
OTTERNESS, IG ;
SEYMOUR, PA ;
GOLDEN, HW ;
REYNOLDS, JA ;
DAUMY, GO .
PHYSIOLOGY & BEHAVIOR, 1988, 43 (06) :797-804
[74]   INTERLEUKIN-1 IN HUMAN OVARIAN-CELLS AND IN PERIPHERAL-BLOOD MONOCYTES INCREASES DURING THE LUTEAL-PHASE - EVIDENCE FOR A MIDCYCLE SURGE IN THE HUMAN [J].
POLAN, ML ;
LOUKIDES, JA ;
HONIG, J .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1994, 170 (04) :1000-1007
[75]   INTERLEUKIN-1-ALPHA INHIBITS PROSTAGLANDIN-E2 RELEASE TO SUPPRESS PULSATILE RELEASE OF LUTEINIZING-HORMONE BUT NOT FOLLICLE-STIMULATING-HORMONE [J].
RETTORI, V ;
GIMENO, MF ;
KARARA, A ;
GONZALEZ, MC ;
MCCANN, SM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (07) :2763-2767
[76]   INTERLEUKIN-1-BETA INHIBITS THE ENDOGENOUS EXPRESSION OF THE EARLY GENE C-FOS LOCATED WITHIN THE NUCLEUS OF LH-RH NEURONS AND INTERFERES WITH HYPOTHALAMIC LH-RH RELEASE DURING PROESTRUS IN THE RAT [J].
RIVEST, S ;
RIVIER, C .
BRAIN RESEARCH, 1993, 613 (01) :132-142
[77]   THE CHRONIC INTRACEREBROVENTRICULAR INFUSION OF INTERLEUKIN-1-BETA ALTERS THE ACTIVITY OF THE HYPOTHALAMIC-PITUITARY-GONADAL AXIS OF CYCLING RATS .1. EFFECT ON LHRH AND GONADOTROPIN BIOSYNTHESIS AND SECRETION [J].
RIVEST, S ;
LEE, S ;
ATTARDI, B ;
RIVIER, C .
ENDOCRINOLOGY, 1993, 133 (06) :2424-2430
[78]   IN THE RAT, INTERLEUKIN-1-ALPHA ACTS AT THE LEVEL OF THE BRAIN AND THE GONADS TO INTERFERE WITH GONADOTROPIN AND SEX STEROID-SECRETION [J].
RIVIER, C ;
VALE, W .
ENDOCRINOLOGY, 1989, 124 (05) :2105-2109
[79]  
RIVIER C, 1990, ENDOCRINOLOGY, V127, P849