Neonatal endotoxin exposure impairs avoidance learning and attenuates endotoxin-induced sickness behavior and central IL-1β gene transcription in adulthood
详细信息 查看全文
- 作者：Rachel A. Kohman ; Andrew J. Tarr ; Nathan L. Sparkman ; Tiroyaone M.H. Bogale ; Gary W. Boehm
- 关键词：Perinatal ; Lipopolysaccharide ; Cytokines ; Interleukin-1 ; Anxiety ; Sickness behavior ; Bacterial endotoxin ; Learning
- 刊名：Behavioural Brain Research
- 出版年：2008
- 出版时间：1 December 2008
- 年：2008
- 卷：194
- 期：1
- 页码：25-31
- 全文大小：521 K
文摘
Infection during infancy, a time of critical neural development, may have long-term implications. Infection or exposure to an immune stimulus such as lipopolysaccharide (LPS) early in life leads to alterations in the reactivity of the hypothalamic–pituitary–adrenal axis (HPA) and febrile response in adulthood. Relatively few studies have assessed the behavioral and cognitive alterations induced by perinatal immune challenge. The data indicate that neonatal immune activation may alter adulthood behavior with, or sometimes without, subsequent adulthood exposure, depending on the study. The current study investigated the behavioral effects and IL-1β transcription following intraperitoneal LPS administration on postnatal days (PNDs) 4 and 5, and subsequent LPS or saline administration in adulthood. Alterations in anxiety, motor behavior, and learning were assessed in male and female subjects. The results indicate that neonatal endotoxin exposure attenuated the LPS-induced decrease in motor behavior in female, but not male, subjects. Furthermore, perinatal immune activation disrupted avoidance learning in male, but not female, subjects in the absence of adulthood LPS administration. In addition, for male subjects, neonatal LPS exposure diminished central IL-1β gene transcription following adulthood LPS administration. These findings indicate that perinatal endotoxin exposure may lead to alterations in the behavioral response to adulthood LPS administration, and provide evidence that early immune activation alone may trigger alterations in adulthood learning ability.