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Fig. 10 | Molecular Brain

Fig. 10

From: Differential arousal regulation by prokineticin 2 signaling in the nocturnal mouse and the diurnal monkey

Fig. 10

Diagram showing the differential arousal regulation by the PK2 signaling of ipRGC onto brain targets. Clock-controlled PK2 is expressed in the ipRGC, the only photic channels that transmit central non-vision functions of light. Overall, the PK2 signaling is stimulatory for the diurnal monkey and inhibitory for the nocturnal mouse, as shown by the antagonist blockade and PK2-deficiency. The differential expression of PKR2 in the retinorecipient ventral SCN and the superficial layer of SC indicates that the PK2 signaling of the ipRGC dominantly funnels through ipRGC-SCN and ipRGC-SC for the mouse and the monkey, respectively. For the nocturnal animals, the arousal stimulation via the ipRGC-SC pathway by light is minor (transient, not sustained), consistent with the absence of PKR2 in the SC of the mouse brain. The PK2 signaling of the ipRGC-SCN pathway is clearly inhibitory for the nocturnal mouse, although it is unclear whether it is inhibitory or stimulatory for the diurnal animals. SC may mediate the light-driven arousal via the ascending projections to cortices that are routed through the lateral posterior/Pulvinar complex of the thalamus. Alternatively, SC may promote arousal via the descending projections to the mesencephalic reticular formation, an important component of the ascending activation system (ref 42–45). Our model indicates that the mammalian diurnal/nocturnal determination is mediated by the differential signaling of the ipRGC onto their brain targets, and thus divergent signaling mechanisms downstream of the SCN may not be necessary. In diurnal animals, upstream clocks such as the ones in the ipRGC likely play more dominant roles than the SCN, at least for arousal regulation under light and dark condition

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