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ARTICLE, Behavioral/Systems/Cognitive

Intrinsic Role of Polysialylated Neural Cell Adhesion Molecule in Photic Phase Resetting of the Mammalian Circadian Clock

Rebecca A. Prosser, Urs Rutishauser, Grace Ungers, Lenka Fedorkova and J. David Glass
Journal of Neuroscience 15 January 2003, 23 (2) 652-658
Rebecca A. Prosser
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Urs Rutishauser
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Grace Ungers
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Lenka Fedorkova
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J. David Glass
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    Fig. 1.

    Circadian variation in the tissue content of PSA in the SCN at different times of the circadian cycle assessed by immunoblot assay. OD, Optic density.n = 3 per time point. Error bars are SEM; *p < 0.05 versus ZT 24 level.

  • Fig. 2.
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    Fig. 2.

    Immunohistochemical staining for PSA in the SCN at ZT 6. The PSA (green labeling) is clearly seen throughout the SCN under normal in vitro conditions (A) but is absent from the SCN after treatment with endo N (B). 3V, Third ventricle; OC, optic chiasm.

  • Fig. 3.
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    Fig. 3.

    Glutamate acutely stimulates PSA expression in the SCN slice. A 10 min application of glutamate induced an ∼200% increase in total SCN PSA content within 30 min of treatment. The PSA levels in untreated controls exhibited a gradual decrease throughout the subjective night. Pretreatment of slices with endo N prevented any glutamate-induced stimulation of PSA. Each time point is an average of three samples. Open circles, Glutamate-treated tissue;filled circles, no treatment; open triangles, glutamate plus endo N-treated tissue.

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    Fig. 4.

    endo N blocks in vitro phase shifts induced by optic chiasm stimulation. Shown are representative single-unit activity recordings from SCN slices after the following treatments: A, no treatment, showing the normal peak in activity at ZT 6; B, optic chiasm stimulation at ZT 14, showing a 3.5 hr phase delay in activity; C, optic chiasm stimulation plus endo N, showing no phase shift; andD, optic chiasm stimulation plus inactive endo N, showing a 3.5 hr phase delay. Horizontal bars, Time of lights-off in the animal colony; vertical bars, times of treatment; dotted lines, mean time of peak neuronal activity in control slices.

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    Fig. 5.

    Histogram plot summarizing the results of phase-shifting experiments. Shown are the mean ± SEM phase shifts induced by the different experimental conditions relative to the mean time-of-peak in control slices (ZT 6.0 ± 0.3;n = 3). Numbers below eachbar indicate the number of replicate experiments. *p < 0.05 versus untreated slices.

  • Fig. 6.
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    Fig. 6.

    endo N blocks in vitro phase shifts induced by glutamate application to the SCN. Shown are representative single-unit activity recordings from SCN slices after the following treatments: A, glutamate (1 mm) at ZT14, showing a 3.5 hr delay in neuronal activity; and B, glutamate (1 mm) plus endo N, showing no phase shift. For details, see Figure 4 legend.

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The Journal of Neuroscience: 23 (2)
Journal of Neuroscience
Vol. 23, Issue 2
15 Jan 2003
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Intrinsic Role of Polysialylated Neural Cell Adhesion Molecule in Photic Phase Resetting of the Mammalian Circadian Clock
Rebecca A. Prosser, Urs Rutishauser, Grace Ungers, Lenka Fedorkova, J. David Glass
Journal of Neuroscience 15 January 2003, 23 (2) 652-658

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Intrinsic Role of Polysialylated Neural Cell Adhesion Molecule in Photic Phase Resetting of the Mammalian Circadian Clock
Rebecca A. Prosser, Urs Rutishauser, Grace Ungers, Lenka Fedorkova, J. David Glass
Journal of Neuroscience 15 January 2003, 23 (2) 652-658
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