In VivoResetting of the Hamster Circadian Clock by 5-HT7Receptors in the Suprachiasmatic Nucleus

Jul 5, 2001The Journal of neuroscience : the official journal of the Society for Neuroscience

Resetting the hamster's internal clock through serotonin receptors in the brain's daily rhythm center

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Abstract

Three-hour perfusions of the SCN with 5-HT or the receptor agonist 8-OH-DPAT advanced the phase of the circadian rhythm in Syrian hamsters.

Phase advances were more than threefold enhanced by pretreatment with the 5-HT synthesis inhibitor para-chlorophenylalanine.
Inhibition of phase advances induced by 8-OH-DPAT was observed with the 5-HT(2,7) receptor antagonist ritanserin and the selective 5-HT(7) receptor antagonist DR4004.
Concurrent light exposure during 8-OH-DPAT perfusion abolished the observed phase advances.
Co-perfusion with TTX, which blocked in vivo 5-HT release, did not suppress the phase advances induced by intra-SCN 8-OH-DPAT.
Results suggest that 5-HT(7) receptor-mediated phase resetting is influenced by postsynaptic responsiveness to 5-HT and photic stimulation.

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Serotonin (5-HT) has been strongly implicated in the regulation of the mammalian circadian clock located in the suprachiasmatic nuclei (SCN); however, its role in behavioral (nonphotic) circadian phase resetting remains elusive. Central to this issue are divergent lines of evidence that the SCN may, or may not, be a target for the phase-resetting effects of 5-HT. We have addressed this question using a novel reverse-microdialysis approach for timed perfusions of serotonergic and other agents to the Syrian hamster SCN with durations equivalent to the increases in in vivo 5-HT release during phase-resetting behavioral manipulations. We found that 3 hr perfusions of the SCN with either 5-HT or the 5-HT(1A,7) receptor agonist 2-dipropylamino-8-hydroxy-1,2,3,4-tetrahydro-naphthalene (8-OH-DPAT) at midday advanced the phase of the free-running circadian rhythm of wheel-running assessed using an Aschoff type II procedure. Phase shifts induced by 8-OH-DPAT were enhanced more than threefold by pretreatment with the 5-HT synthesis inhibitor para-chlorophenylalanine. Phase advances induced by SCN 8-OH-DPAT perfusion were significantly inhibited by the 5-HT(2,7) receptor antagonist ritanserin and by the more selective 5-HT(7) receptor antagonist DR4004, implicating the 5-HT(7) receptor in mediating this phase resetting. Concurrent exposure to light during the 8-OH-DPAT perfusion abolished the phase advances. Furthermore, coperfusion of the SCN with TTX, which blocked in vivo 5-HT release, did not suppress intra-SCN 8-OH-DPAT-induced phase advances. These results indicate that 5-HT(7) receptor-mediated phase resetting in the SCN is markedly influenced by the degree of postsynaptic responsiveness to 5-HT and by photic stimulation. Finally, 5-HT may act directly on SCN clock cells to induce in vivo nonphotic phase resetting.

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In VivoResetting of the Hamster Circadian Clock by 5-HT7Receptors in the Suprachiasmatic Nucleus

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