Effects of phototherapy on memory and BDNF/TrkB signaling pathway in sleep-deprived mice

Sleep disorder is a common clinical disease that easily induces and aggravates cognitive disorders, especially the decline in learning and memory ability. In recent years, phototherapy has been widely studied as a non-invasive, safe, and less side-effect physical therapy method. Phototherapy may become an effective treatment for sleep disorders. In this study, we investigated the effects of phototherapy on learning and memory in sleep deprivation model mice, and to investigate the effects of phototherapy on inflammatory response, oxidative stress and the brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B(TrkB)signaling pathway in sleep-deprived mice. The mice were randomly divided into 3 groups: control group, sleep deprivation group and phototherapy group (468 nm, 100 lux, 300 lux and 900 lux). The results showed that sleep deprivation led to an increase in swim latency and a lower number of platform crossings, promoted the expression of tumor necrosis factor-alpha(TNF-α), decreased the expression of superoxide dismutase(SOD) activity, and decreased the mRNA expression of BDNF, TrkB, and Akt. After phototherapy, the phototherapy group had a shorter swimming latency, higher number of plateau crossings, decreased the expression of TNF-α, increased expression of SOD. The mRNA expression of BDNF, TrkB, and Akt increased, and the effect of 300 lux light dose was more significant. Therefore, phototherapy can repair the oxidative stress damage caused by sleep deprivation, regulate the inflammatory response, promote the expression of BDNF to compensate for the relatively short period of sleep deprivation, protect their cognitive ability, and alleviate the learning and memory deficits caused by sleep deprivation.