University of Delaware, Department of Psychological and Brain Sciences, 105 The Green, Newark, DE, 19716, United States.
Behav Brain Res. 2021 Oct 11;415:113449. doi: 10.1016/j.bbr.2021.113449. Epub 2021 Jul 9.
Many individuals diagnosed with neuropsychiatric disorders, such as autism, attention-deficit/hyperactivity disorder, schizophrenia, and social anxiety disorder, all share a common dimension of aberrant social behavior. Epidemiological data indicate that adverse environmental factors contribute to the risk for neurodevelopmental disorders, including those associated with aberrant social behavior. Early-life exposure to infectious pathogens is one of those adverse environmental factors, suggesting that activation of the immune system during early development may contribute to disease pathology associated with altered social behavior. In the current project, we examined the impact of neonatal infection, with or without juvenile immune activation, on the expression of juvenile social behavior and on the expression of inflammatory cytokines and microglial signaling molecules in the juvenile rat brain. The outcomes of these experiments revealed that neonatal infection significantly decreased juvenile social interaction, but significantly increased juvenile play behavior in male and female rats. Moreover, neonatal infection alone, juvenile immune activation alone, and neonatal infection plus juvenile immune activation all significantly impaired social recognition in juvenile male rats. Juvenile female rats (including controls) did not demonstrate social recognition as measured in our three-chamber social recognition test. Taken together, the behavioral and molecular data presented here support the sensitivity of the developing brain to immune activation, particularly in the expression of age-appropriate social behaviors. These data warrant the design of additional studies to examine the mechanistic relationship between early-life immune activation and aberrant social behavior to develop novel as well as modify existing therapeutic targets and preventative measures to help those who display aberrant social behavior.
许多被诊断患有神经精神疾病的个体,如自闭症、注意缺陷/多动障碍、精神分裂症和社交焦虑症,都存在共同的异常社交行为维度。流行病学数据表明,不良的环境因素会增加神经发育障碍的风险,包括与异常社交行为相关的障碍。生命早期暴露于传染性病原体是这些不良环境因素之一,这表明早期发育过程中免疫系统的激活可能与改变社交行为相关的疾病病理有关。在当前的项目中,我们研究了新生儿感染,以及是否存在青少年免疫激活,对青少年社交行为的表达以及青少年大鼠大脑中炎症细胞因子和小胶质细胞信号分子的表达的影响。这些实验的结果表明,新生儿感染显著降低了青少年的社交互动,但显著增加了雄性和雌性大鼠的青少年玩耍行为。此外,新生儿感染本身、青少年免疫激活本身以及新生儿感染加青少年免疫激活都显著损害了雄性幼鼠的社会识别能力。幼鼠雌性(包括对照组)在我们的三箱社交识别测试中没有表现出社交识别。总的来说,这里呈现的行为和分子数据支持发育中大脑对免疫激活的敏感性,特别是在适当年龄的社交行为表达方面。这些数据需要设计更多的研究来检查早期生活免疫激活与异常社交行为之间的机制关系,以开发新的和修改现有的治疗靶点和预防措施,帮助那些表现出异常社交行为的人。