Daily restricted feeding (RF) can produce food-entrainable oscillations in both intact and suprachiasmatic nucleus (SCN)-lesioned animals. Thus, there are two circadian rhythms, one of which is SCN-dependent and the other SCN-independent. Recently, it has been established that several mouse clock genes, such as mPer1, mPer2 and mPer3 are expressed in the SCN and other brain tissues. Although the role of mPer genes expressed in the SCN has recently been evaluated in the SCN-dependent rhythm, their function in the SCN-independent rhythm is still poorly understood. In order to understand the role of these genes in SCN-independent rhythm, we examined the expression pattern of mPer1 and mPer2 mRNA in each brain area of mice under RF. Mice were allowed access to food for 4 h during either the daytime under a light-dark cycle or the subjective daytime under constant dark. After 6 days of scheduled RF, the night-time or subjective night-time peak of mPer mRNA changed to a daytime peak in the cerebral cortex and hippocampus, with moderate expression in the striatum, pyriform cortex and paraventricular nucleus, and no expression in the SCN. The daytime peak in the cerebral cortex returned to a night-time peak after the release of RF to a free-feeding schedule. Although the basal rhythm of mPer expression disappeared in SCN-lesioned mice, RF produced mPer mRNA rhythm in the cerebral cortex of these mice. The present results provide evidence of an association between food-entrainable oscillations and the expression of mPer1 and mPer2 in the cerebral cortex and hippocampus.

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Aging alters circadian components such as the free-running period, the day-to-night activity ratio and photic entrainment in behavioral rhythms, and 2-deoxyglucose uptakes and neuronal firing in the suprachiasmatic nucleus (SCN). A core clock mechanism in the mouse SCN appears to involve a transcriptional feedback loop in which Period (Per) and Cryptochrome (Cry) genes play a role in negative feedback. The circadian rhythm systems include photic entrainment, clock oscillation, and outputs of clock information such as melatonin production. In this experiment, we examined clock gene expression to determine whether circadian input, oscillation, and output are disrupted with aging. Circadian expression profiles of rPer1, rPer2, or rCry1 mRNA were very similar in the SCN, the paraventricular nucleus of the hypothalamus (PVN), and the pineal body of young and aged (22-26 months) rats. On the other hand, the photic stimulation-induced rapid expression of Per1 and Per2 in the SCN was reduced with aging. The present results suggest that the molecular mechanism of clock oscillation in the SCN, PVN, and pineal body is preserved against aging, whereas the impairment of Per1 induction in the SCN after light stimulation may result in impaired behavioral photic entrainment in aged rats.

1 Serotonergic projections from the midbrain raphe nuclei to the suprachiasmatic nuclei (SCN) are known to regulate the photic entrainment of circadian clocks. However, it is not known which 5-hydroxytryptamine (5-HT) receptor subtypes are involved in the circadian regulation. In order to verify the role of 5-HT 1A receptors, we examined the e ects of 5-{3-[((2S)-1,4-benzodioxan-2-ylmethyl)amino]-propoxy}-1,3-benzodioxole HCl (MKC-242), a selective 5-HT 1A receptor agonist, on photic entrainment of wheel-running circadian rhythms of hamsters. 2 MKC-242 (3 mg kg 71 , i.p.) signi®cantly accelerated the re-entrainment of wheel-running rhythms to a new 8 h delayed or advanced light-dark cycle.

Aging alters circadian components such as the free-running period, the day-to-night activity ratio and photic entrainment in behavioral rhythms, and 2-deoxyglucose uptakes and neuronal firing in the suprachiasmatic nucleus (SCN). A core clock mechanism in the mouse SCN appears to involve a transcriptional feedback loop in which Period (Per) and Cryptochrome (Cry) genes play a role in negative feedback. The circadian rhythm systems include photic entrainment, clock oscillation, and outputs of clock information such as melatonin production. In this experiment, we examined clock gene expression to determine whether circadian input, oscillation, and output are disrupted with aging. Circadian expression profiles of rPer1, rPer2, or rCry1 mRNA were very similar in the SCN, the paraventricular nucleus of the hypothalamus (PVN), and the pineal body of young and aged (22-26 months) rats. On the other hand, the photic stimulation-induced rapid expression of Per1 and Per2 in the SCN was reduced with aging. The present results suggest that the molecular mechanism of clock oscillation in the SCN, PVN, and pineal body is preserved against aging, whereas the impairment of Per1 induction in the SCN after light stimulation may result in impaired behavioral photic entrainment in aged rats.