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The Journal of Neuroscience, October 15, 2000, 20(20):7830-7837

Differential cAMP Gating of Glutamatergic Signaling Regulates Long-Term State Changes in the Suprachiasmatic Circadian Clock

Shelley A. Tischkau^{1, 3}, Eve A. Gallman¹, Gordon F. Buchanan², and Martha U. Gillette^{1, 2, 3}

Departments of ¹ Cell and Structural Biology, ² Molecular and Integrative Physiology, and ³ the Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801

We investigated a role for cAMP/protein kinase A (PKA) in light/glutamate (GLU)-stimulated state changes of the mammalian circadian clock in the suprachiasmatic nucleus (SCN). Nocturnal GLU treatment elevated [cAMP]; however, agonists of cAMP/PKA did not mimic the effects of light/GLU. Coincident activation of cAMP/PKA enhanced GLU-stimulated state changes in early night but blocked light/GLU-induced state changes in the late night, whereas inhibition of cAMP/PKA reversed these effects. These responses are distinct from those mediated by mitogen-activated protein kinase (MAPK). MAPK inhibitors attenuated both GLU-induced state changes. Although GLU induced mPer1 mRNA in both early and late night, inhibition of PKA blocked this event only in early night, suggesting that cellular mechanisms regulating mPer1 are gated by the suprachiasmatic circadian clock. These data support a diametric gating role for cAMP/PKA in light/GLU-induced SCN state changes: cAMP/PKA promotes the effects of light/GLU in early night, but opposes them in late night.

Key words: suprachiasmatic nucleus; glutamate; signal transduction; mPer1; protein kinase A; MAP kinase; rat

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Copyright © 2000 Society for Neuroscience  0270-6474/00/20207830-08$05.00/0

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