Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is characterized by disabling fatigue of at least 6 months, in addition to symptoms such as muscle pain and muscle weakness. There is no treatment provides long-term benefits to most patients. Recently, clinical research suggested the involvement of pyruvate dehydrogenase (PDH) in ME/CFS. PDH is a crucial enzyme in the mitochondria matrix that links glycolysis to the tricarboxylic acid cycle and oxidative phosphorylation. However, it is little known whether PDH could be a therapeutic target. The purpose of this study was to establish ME/CFS in mice and to investigate the involvement of PDH in ME/CFS. To induce the chronic fatigue in mice, a repeated forced swimming test was conducted. To evaluate fatigue, we measured immobility time in forced swimming test and starting time of grooming. An open field test was conducted on day 8. After 25 d of the forced swimming test, the mitochondrial fraction in gastrocnemius muscle was isolated and PDH activity was measured. Moreover, we evaluated the effect of PDH activation by administering sodium dichloroacetate (DCA). In ME/CFS mice group, the immobility time and starting time of grooming increased time-dependently. In addition, the moved distance was decreased in ME/CFS mice. PDH activity was decreased in the mitochondrial fraction of the gastrocnemius muscle of the forced swimming group. DCA treatment may be beneficial in preventing fatigue-like behavior in ME/CFS. These findings indicate that ME/CFS model was established in mice and that a decrease in mitochondrial PDH activity is involved with the symptom of ME/CFS.
In the present study, we investigated whether blue light emission diode (LED) light exposure affects the maternal behavior of mice. The brain function of the offspring mice, including short-term memory, locomotor activity, anxiety-like behavior, and depression-like behavior, was evaluated. Pregnant mice at day 11 were housed in the apparatus for exposure to blue LED light during the daytime. Nesting behavior and the survival of pups were observed until weaning. After weaning, the offspring mice were bred in normal light conditions until 12 weeks old, and then the Y-maze test, open field test, and tail suspension test were performed. Retinal functions were evaluated by electroretinogram and histological analysis. Blue LED light exposure during the daytime induced retinal damage, but did not affect behavior related to maternal care in maternal mice. In the offspring mice, blue LED light exposure during the daytime did not affect the retina or brain functions. These findings suggest that blue LED light during the daytime might not be a risk factor for disruption of the mother-infant relationship or offspring brain development in mice.
White light emitting diode (LED) lighting is being used more frequently for illumination in recent years. The coupling of blue with yellow emitting phosphors produces white LED light. Blue light has a short wavelength in the visible light spectrum and exerts a strong influence on photobiological functions. Cycling light exposure is necessary for the synchronizing the circadian rhythm. The exposure to white light at subjective nighttime induces cognitive impairment, depression, and anxiety by disturbing the circadian rhythm and increasing stress hormone. However, few studies have been performed at the subjective daytime. Thus, the aim of this study was to determine whether exposure to blue light from an LED at subjective daytime affects brain function. We irradiated C57BL/6J mice with 200 lux of blue LED light for 12 h/day for 6 weeks at the subjective daytime and performed Y-maze, object recognition, tail suspension, and open field tests. There was no significant difference between the exposed mice and control mice. Histological analysis of the retina showed that the blue light exposure did not alter the retinal thickness. We conclude that the exposure to blue LED light at subjective daytime does not affect the retinal morphology or brain function in pigmented mice.
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