Light and glutamate-induced degradation of the circadian oscillating protein BMAL1 during the mammalian clock resetting

Recently discovered mammalian clock genes are believed to compose the core oscillator, which generates the circadian rhythm. BMAL1/CLOCK heterodimer i s the essential positive element that drives clock-related transcription an d self-sustaining oscillation by a negative feedback mechanism. We examined BMAL1 protein expression in the rat suprachiasmatic nuclei (SCN) by immuno blot analysis. Anti-BMAL1 antiserum raised against rBMAL1 recognized 70 kDa mBMAL1b and detected a similar immunoreactivity (IR) as a major band in ra t brains. Robust circadian BMAL1-IR oscillations with nocturnal peaks were detected in the SCN during a light/dark cycle and under constant darkness. A short duration light exposure at night acutely reduced BMAL1-IR in the SC N during photoentrainment. This might be attributable to the degradation of BMAL1 protein. Application of glutamate and NMDA to the SCN slices at proj ected night, a procedure mimicking photic phase delay shift, also acutely r educed BMAL1-IR in a similar manner. A rapid decrease of BMAL1 protein sugg ests that BMAL1 protein might be implicated in the light-transducing pathwa y within the SCN.