Morphological approach to the light entrainment mechanism of the circadian clock

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Nocturnal light induces Perl and Per2 genes, which leads to resetting of the circadian clock in the suprachiasmatic nucleus (SCN), the mammalian circadian center. We investigated the light resetting mechanism of their circadian clocks. By using in situ hybridization technique, we found that Perl is used for the advance of the clock and Per2 is used for the delay. Next, in mammals, light is the primary environmental signal used to synchronize endogenous rhythms to the environment. Daylength, or photoperiod also affects many physiological events such as locomotor activity, sleep-wake rhythms, temperature and hormonal secretion. We examined the effects of photoperiod on the daily expression of Perl gene in the SCN. We suggested that the change of photoperiod affected not only in the VLSCN that has rich projection from the retina but also in the DMSCN that is absent from the direct retinal projection. Also, we observed that desynchronization underlies the multicell-level amplitude decrease in the rat suprachiasmatic nucleus induced by critical light pulses.Using in situ hybridization methods, we investigated the localization of Prokineticin (PK2) and prokineticin receptor 2 (PKR2) in the rat SCN. PK2 mRNA-positive neurons were scattered in both the dorsomedial and ventrolateral SCN. In contrast, PKR2 mRNA-containing neurons were clustered in the dorsolateral part of the SCN. Then, to examine the role of PKR2 in the SCN, we created PKR2-gene-disrupted mice (Pkr2(-/-)). Phenotypic analysis indicated that Pkr2(-/-) mice exhibited hypoplasia of the OB. In addition, the Pkr2(-/-) mice showed severe atrophy of the reproductive system. In the Pkr2(-/-) mice, Immunohistochemical analysis revealed that gonadotropin-releasing hormone neurons were absent in the hypothalamus in the Pkr2(-/-) mice. The phenotype of the Pkr2(-/-) mice showed similarity to the clinical features of Kallmann syndrome.