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The Journal of Neuroscience, February 1, 1999, 19(3):1115-1121

Inhibition of Light- or Glutamate-Induced mPer1 Expression Represses the Phase Shifts into the Mouse Circadian Locomotor and Suprachiasmatic Firing Rhythms

Masashi Akiyama1, Yasuko Kouzu1, Satomi Takahashi1, Hisanori Wakamatsu1, Takahiro Moriya2, Miyuki Maetani3, Shigenori Watanabe3, Hajime Tei4, Yoshiyuki Sakaki4, and Shigenobu Shibata1, 2

1 Department of Pharmacology and Brain Science and 2 ARCHS, School of Human Sciences, Waseda University, Tokorozawa, Saitama 359-1192, Japan, 3 Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-82, Japan, and 4 Human Genome Center, Institute of Medical Sciences, University of Tokyo, Tokyo, Japan

mPer1, a mouse gene, is a homolog of the Drosophila clock gene period and has been shown to be closely associated with the light-induced resetting of a mammalian circadian clock. To investigate whether the rapid induction of mPer1 after light exposure is necessary for light-induced phase shifting, we injected an antisense phosphotioate oligonucleotide (ODN) to mPer1 mRNA into the cerebral ventricle. Light-induced phase delay of locomotor activity at CT16 was significantly inhibited when the mice were pretreated with mPer1 antisense ODN 1 hr before light exposure. mPer1 sense ODN or random ODN treatment had little effect on phase delay induced by light pulses. In addition, glutamate-induced phase delay of suprachiasmatic nucleus (SCN) firing rhythm was attenuated by pretreatment with mPer1 antisense ODN, but not by random ODN. The present results demonstrate that induction of mPer1 mRNA is required for light- or glutamate-induced phase shifting, suggesting that the acute induction of mPer1 mRNA in the SCN after light exposure is involved in light-induced phase shifting of the overt rhythm.

Key words: antisense oligonucleotide; circadian rhythm; firing rhythm; mPer1; phase shift; suprachiasmatic nucleus

Copyright © 1999 Society for Neuroscience  0270-6474/99/1931115-07$05.00/0


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