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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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