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Keywords:

  • behavioral rhythm;
  • DBP;
  • Per1;
  • Per2;
  • rat

Abstract

Chronic treatment with methamphetamine (MAP) in rats increases the amplitude of locomotor activity rhythm and desynchronizes the activity rhythm from a light–dark cycle. In MAP-treated animals the circadian rhythms in clock gene expressions in the parietal cortex and caudate putamen (CPU) desynchronized from those in the suprachiasmatic nucleus (SCN), the site of a circadian clock. In order to determine whether the 24-h pattern of clock gene expression was due to direct responses of clock genes to MAP treatment or to the oscillations uncoupled or induced by MAP, MAP treatment was terminated when the activity phase of MAP-treated rats was completely desynchronized from a light–dark cycle. In spite of MAP withdrawal, the behavioral as well as Per1, Per2 and DBP expression rhythms in the parietal cortex and CPU still persisted for at least one cycle. However, the rhythm amplitudes were substantially decreased in Per1 and Per2 expression. In contrast, the circadian rhythm of DBP expressions persisted without damping. These data indicate that chronic MAP treatment induced circadian oscillations in Per1 and Per2, in the parietal cortex and CPU, in parallel with the locomotor activity rhythm.