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Short-term acute bright light exposure induces a prolonged anxiogenic effect in mice via a retinal ipRGC-CeA circuit

Light modulates mood through various retina-brain pathways. We showed that mice treated with short-term acute bright light exposure displayed anxiety-related phenotypes in a prolonged manner even after the termination of the exposure. Such a postexposure anxiogenic effect depended upon melanopsin-ba...

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Detalles Bibliográficos
Autores principales: Wang, Ge, Liu, Yun-Feng, Yang, Zhe, Yu, Chen-Xi, Tong, Qiuping, Tang, Yu-Long, Shao, Yu-Qi, Wang, Li-Qin, Xu, Xun, Cao, Hong, Zhang, Yu-Qiu, Zhong, Yong-Mei, Weng, Shi-Jun, Yang, Xiong-Li
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Association for the Advancement of Science 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10032603/
https://www.ncbi.nlm.nih.gov/pubmed/36947616
http://dx.doi.org/10.1126/sciadv.adf4651
Descripción
Sumario:Light modulates mood through various retina-brain pathways. We showed that mice treated with short-term acute bright light exposure displayed anxiety-related phenotypes in a prolonged manner even after the termination of the exposure. Such a postexposure anxiogenic effect depended upon melanopsin-based intrinsically photosensitive retinal ganglion cell (ipRGC) activities rather than rod/cone photoreceptor inputs. Chemogenetic manipulation of specific central nuclei demonstrated that the ipRGC–central amygdala (CeA) visual circuit played a key role in this effect. The corticosterone system was likely to be involved in this effect, as evidenced by enhanced expression of the glucocorticoid receptor (GR) protein in the CeA and the bed nucleus of the stria terminalis and by the absence of this effect in animals treated with the GR antagonist. Together, our findings reveal a non-image forming visual circuit specifically designed for “the delayed” extinction of anxiety against potential threats, thus conferring a survival advantage.