PT - JOURNAL ARTICLE AU - Teruya Tamaru AU - Yasushi Isojima AU - Takashi Yamada AU - Masato Okada AU - Katsuya Nagai AU - Ken Takamatsu TI - Light and Glutamate-Induced Degradation of the Circadian Oscillating Protein BMAL1 during the Mammalian Clock Resetting AID - 10.1523/JNEUROSCI.20-20-07525.2000 DP - 2000 Oct 15 TA - The Journal of Neuroscience PG - 7525--7530 VI - 20 IP - 20 4099 - http://www.jneurosci.org/content/20/20/7525.short 4100 - http://www.jneurosci.org/content/20/20/7525.full SO - J. Neurosci.2000 Oct 15; 20 AB - Recently discovered mammalian clock genes are believed to compose the core oscillator, which generates the circadian rhythm. BMAL1/CLOCK heterodimer is the essential positive element that drives clock-related transcription and self-sustaining oscillation by a negative feedback mechanism. We examined BMAL1 protein expression in the rat suprachiasmatic nuclei (SCN) by immunoblot analysis. Anti-BMAL1 antiserum raised against rBMAL1 recognized 70 kDa mBMAL1b and detected a similar immunoreactivity (IR) as a major band in rat 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 SCN during photoentrainment. This might be attributable to the degradation of BMAL1 protein. Application of glutamate and NMDA to the SCN slices at projected night, a procedure mimicking photic phase delay shift, also acutely reduced BMAL1-IR in a similar manner. A rapid decrease of BMAL1 protein suggests that BMAL1 protein might be implicated in the light-transducing pathway within the SCN.