Adolescent sleep shapes social novelty preference in mice.

Adolescent sleep shapes social novelty preference in mice.
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青春期睡眠塑造小鼠的社会新奇偏好。

DOI:
10.1038/s41593-022-01076-8
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发表时间:
2022-07
影响因子:
25
通讯作者:
de Lecea, Luis
de Lecea, Luis
中科院分区:
医学1区
文献类型:
--
作者:
Bian, Wen-Jie;Brewer, Chelsie L.;Kauer, Julie A.;de Lecea, Luis

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睡眠障碍经常发生在神经发育障碍,如自闭症,但睡眠的发育作用在很大程度上是未探索的,发育性睡眠缺陷和他们的行为后果在成年期之间的因果关系仍然难以捉摸。在这里,我们表明,在小鼠中,青春期的睡眠中断(SD),而不是在成年期,会导致社会新奇偏好的长期损害。此外,青少年SD改变了腹侧被盖区(VTA)多巴胺能神经元的激活和释放模式,以响应社会新奇感。这种发育性睡眠功能是由青春期平衡的腹侧被盖区活动介导的;化学遗传性兴奋模仿,而沉默则挽救青少年SD的社交缺陷。最后,我们表明,在Shank 3突变小鼠,改善睡眠或纠正VTA活动在青春期改善成年社会缺陷。总之,我们的研究结果确定了睡眠和多巴胺能活动在社会互动行为发展中的关键作用。
Sleep disturbances frequently occur in neurodevelopmental disorders such as autism, but the developmental role of sleep is largely unexplored, and a causal relationship between developmental sleep defects and their behavioral consequences in adulthood remains elusive. Here we show that in mice, sleep disruption (SD) in adolescence, but not in adulthood, causes long-lasting impairment in social novelty preference. Furthermore, adolescent SD alters the activation and release patterns of dopaminergic neurons in the ventral tegmental area (VTA) in response to social novelty. This developmental sleep function is mediated by balanced VTA activity during adolescence; chemogenetic excitation mimics whereas silencing rescues the social deficits of adolescent SD. Finally, we show that in Shank3 mutant mice, improving sleep or rectifying VTA activity during adolescence ameliorates adult social deficits. Together, our results identify a critical role of sleep and dopaminergic activity in the development of social interaction behavior.
DOI: 10.1038/nn.4593
发表时间: 2017-08
影响因子: 25
作者:
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