Glycine is now used as a chemical for promotion of sleep in humans. It has been demonstrated that glycine administration up to 2g/kg causes the increase of NREM sleep in sleep disturbed rat and hypothermia (0.6 C decrease) in rat. The administration of benzodiazepine not only caused the sleep but affected the circadian rhythm; it blocked the light-induced phase advance of activity rhythm and elevation of Per1 gene expression in the suprachiasmatic nucleus (SCN) in hamsters. In the present experiment, we examined the possibility whether glycine affect light-induced phase shift and c-fos expression in the SCN and retina of mice. Glycine dose-dependently decreased the body temperature of mice (1C decrease with 2 g/kg). After extended light exposure for 2 hrs in the night under LD cycle mouse was kept under constant dark condition. Glycine (0.5-2 g/kg) pretreatment before light exposure dose-dependently attenuated light-induced phase delay. Glycine (2g/kg) pretreatment slightly attenuated light-induced increase of Fos immunoreactivity in the mouse SCN. Further experiment should elucidate whether glycine administration itself causes the phase shift or not. The present results suggest that high dose of glycine may attenuate the light-induced phase shift of circadian clock. [J Physiol Sci. 2008;58 Suppl:S90]