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The Journal of Neuroscience, October 15, 2000, 20(20):7525-7530

Light and Glutamate-Induced Degradation of the Circadian Oscillating Protein BMAL1 during the Mammalian Clock Resetting

Teruya Tamaru¹, Yasushi Isojima², Takashi Yamada¹, Masato Okada², Katsuya Nagai², and Ken Takamatsu¹

¹ Department of Physiology, Toho University School of Medicine, Tokyo 143-8540, Japan and ² Division of Protein Metabolism, Institute for Protein Research, Osaka University, Osaka 565-0871, Japan

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.

Key words: circadian clock; light; phase shift; glutamate; NMDA; suprachiasmatic nucleus

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Copyright © 2000 Society for Neuroscience  0270-6474/00/20207525-06$05.00/0

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