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Maternal immune activation alters visual acuity and retinogeniculate axon pruning in offspring mice
Brain, Behavior, and Immunity ( IF 8.8 ) Pub Date : 2020-10-01 , DOI: 10.1016/j.bbi.2020.08.017
Jinshuai Ren 1 , Yixiu Yan 2 , Shan Cheng 1 , Jianmei Long 1 , Hanxiong Zhang 1 , Junlu Wang 2 , Yi Shen 1 , Yu-Dong Zhou 3 , Matthew P Anderson 4
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Individuals with autism spectrum disorder (ASD) have been found to have a variety of sensory processing deficits. Here we report that maternal immune activation, a known factor for ASD, impairs visual acuity in the offspring mice. By intraperitoneally injecting polyinosinic-polycytidylic acid (polyI:C) to induce maternal immune activation during embryonic days 10 to 14, we found that polyI:C treatment impairs visual acuity in young adult offspring mice as examined by their optomotor responses. Concurrently, polyI:C treatment suppresses retinogeniculate axon elimination, resulting in a high fraction of weak optical fibers innervating the relay neurons in the visual thalamus. The results link in-utero maternal inflammation to defective optical fiber pruning and arrested developmental strengthening of single optic fibers which may underlie impaired visual acuity.

中文翻译:

母体免疫激活改变后代小鼠的视力和视网膜轴突修剪

已发现患有自闭症谱系障碍 (ASD) 的个体具有多种感觉处理缺陷。在这里,我们报告母体免疫激活(ASD 的已知因素)会损害后代小鼠的视力。通过腹膜内注射聚肌苷酸 (polyI:C) 以在胚胎第 10 天到第 14 天诱导母体免疫激活,我们发现 polyI:C 治疗会损害年轻成年后代小鼠的视敏度,如通过它们的视运动反应检查。同时,polyI:C 处理抑制视网膜原性轴突消除,导致大量弱光纤支配视觉丘脑中的中继神经元。
更新日期:2020-10-01
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