Seasonal changes of daylength (photoperiod) affect the expression of hormonal and behavioral circadian rhythms in a variety of organisms. In mammals, such effects might reflect photoperiodic changes in the circadian pacemaking system [located in the suprachiasmatic nucleus (SCN) of the hypothalamus] that governs these rhythms, but to date no functionally relevant, intrinsic property of the SCN has been shown to be photoperiod dependent. We have analyzed the temporal regulation of light-induced c-fos gene expression in the SCN of rats maintained in long or short photoperiods. Both in situ hybridization and immunohistochemical assays show that the endogenous circadian rhythm of light responsiveness in the SCN is altered by photoperiod, with the duration of the photosensitive subjective night under the short photoperiod 5-6 h longer than under the long photoperiod. Our results provide evidence that a functional property of the SCN is altered by photoperiod and suggest that the nucleus is involved in photoperiodic time measurement. Over the course of the year, most mammals respond to seasonal changes of daylength (photoperiod) with altered physiology and behavior. Photoperiodic information from the environment is conveyed to the organism by a circadian rhythm of melatonin production in the pineal gland (1-4). In the rat, rhythmic melatonin production is driven by a circadian rhythm of the activity of pineal N-acetyltransferase (NAT), which synthesizes the melatonin precursor N-acetylserotonin (5, 6). The NAT rhythm is controlled by a light-entrainable circadian pacemaking system in the suprachiasmatic nucleus (SCN) of the hypothalamus; SCN lesions abolish this rhythm (7). Norepinephrine released at night from sympathetic nerve endings in the pineal gland stimulates adrenergic receptors and the cAMP pathway; the resulting induction and activation of pineal NAT activity leads to high nighttime melatonin levels (8). In the rat, the NAT rhythm is entrained to the 24-h light-dark (LD) cycle primarily by light onset at dawn (9). With longer daylengths, light at an earlier dawn advances the phase of the morning NAT decline, while light at a later dusk delays the phase of the evening NAT rise (3, 10). The resulting alteration in the duration of the nocturnal melatonin signal, compressed during long summer days and decompressed during short winter days, appears to serve as an endogenous photoperiodic message (2,3,11).When rats and hamsters are transferred from a long to a short photoperiod, the decompression of the melatonin signal occurs gradually (12-14). Since high NAT activity can be induced independent of the photoperiod by administration of a ,B-adrenergic agonist (15), it seems likely that the neural substrate for this gradual decompression lies upstream of the pineal gland, perhaps in the SCN. Importantly, another circadian rhythm governed by the SCN is photoperiodic. The duration of nocturnal locomotor activity (a) in hamsters is also compressed during long days and decompressed during short days (16, 17)...
The vertebrate circadian clock was thought to be highly localized to specific anatomical structures: the mammalian suprachiasmatic nucleus (SCN), and the retina and pineal gland in lower vertebrates. However, recent findings in the zebrafish, rat and in cultured cells have suggested that the vertebrate circadian timing system may in fact be highly distributed, with most if not all cells containing a clock. Our understanding of the clock mechanism has progressed extensively through the use of mutant screening and forward genetic approaches. The first vertebrate clock gene was identified only a few years ago in the mouse by such an approach. More recently, using a syntenic comparative genetic approach, the molecular basis of the the tau mutation in the hamster was determined. The tau gene in the hamster appears to encode casein kinase 1 epsilon, a protein previously shown to be important for PER protein turnover in the Drosophila circadian system. A number of additional clock genes have now been described. These proteins appear to play central roles in the transcription-translation negative feedback loop responsible for clock function. Post-translational modification, protein dimerization and nuclear transport all appear to be essential features of how clocks are thought to tick.
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