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The Journal of Neuroscience, July 9, 2003, 23(14):6141-6151

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An Abrupt Shift in the Day/Night Cycle Causes Desynchrony in the Mammalian Circadian Center

Mamoru Nagano,1 Akihito Adachi,1 Ken-ichi Nakahama,1 Toru Nakamura,2 Masako Tamada,3 Elizabeth Meyer-Bernstein,4 Amita Sehgal,4 and Yasufumi Shigeyoshi1

1Department of Anatomy and Neurobiology, Kinki University School of Medicine, Osakasayama City, Osaka 589-8511, Japan, 2Department of Dentistry, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan, 3Department of Anesthesiology, Kobe University School of Medicine, Kobe 650-0017 Japan, and 4Howard Hughes Medical Institute, Department of Neuroscience, University of Pennsylvania Medical School, Philadelphia, Pennsylvania 19104

The suprachiasmatic nucleus (SCN) is the neuroanatomical locus of the mammalian circadian pacemaker. Here we demonstrate that an abrupt shift in the light/dark (LD) cycle disrupts the synchronous oscillation of circadian components in the rat SCN. The phases of the RNA cycles of the period genes Per1 and Per2 and the cryptochrome gene Cry1 shifted rapidly in the ventrolateral, photoreceptive region of the SCN, but were relatively slow to shift in the dorsomedial region. During the period of desynchrony, the animals displayed increased nighttime rest, the timing of which was inversely correlated with the expression of Per1 mRNA in the dorsomedial SCN. Molecular resynchrony required ~6 d after a 10 hr delay and 9~13 d after a 6 hr advance of the LD cycle and was accompanied by the reemergence of normal rest–activity patterns. This dissociation and slow resynchronization of endogenous oscillators within the SCN after an LD cycle shift suggests a mechanism for the physiological symptoms that constitute jet lag.

Key words: suprachiasmatic nucleus; jet lag; Per1; Per2; Cry1; desynchrony; resynchronization

Received Jan. 28, 2003; revised Apr. 29, 2003; accepted May. 8, 2003.




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