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The Journal of Neuroscience, October 1, 1999, 19(19):8630-8636

Circadian Rhythms in the Suprachiasmatic Nucleus are Temperature-Compensated and Phase-Shifted by Heat Pulses In Vitro

Norman F. Ruby, D. Erik Burns, and H. Craig Heller

Department of Biological Sciences, Stanford University, Stanford, California 94305

Temperature compensation and the effects of heat pulses on rhythm phase were assessed in the suprachiasmatic nucleus (SCN). Circadian neuronal rhythms were recorded from the rat SCN at 37 and 31°C in vitro. Rhythm period was 23.9 ± 0.1 and 23.7 ± 0.1 hr at 37 and 31°C, respectively; the Q₁₀ for tau was 0.99. Heat pulses were administered at various circadian times (CTs) by increasing SCN temperature from 34 to 37°C for 2 hr. Phase delays and advances were observed during early and late subjective night, respectively, and no phase shifts were obtained during midsubjective day. Maximum phase delays of 2.2 ± 0.3 hr were obtained at CT 14, and maximum phase advances of 3.5 ± 0.2 hr were obtained at CT 20. Phase delays were not blocked by a combination of NMDA [AP-5 (100 µM)] and non-NMDA [CNQX (10 µM)] receptor antagonists or by tetrodotoxin (TTX) at concentrations of 1 or 3 µM. The phase response curve for heat pulses is similar to ones obtained with light pulses for behavioral rhythms. These data demonstrate that circadian pacemaker period in the rat SCN is temperature-compensated over a physiological range of temperatures. Phase delays were not caused by activation of ionotropic glutamate receptors, release of other neurotransmitters, or temperature-dependent increases in metabolism associated with action potentials. Heat pulses may have phase-shifted rhythms by directly altering transcriptional or translational events in SCN pacemaker cells.

Key words: suprachiasmatic; circadian; temperature compensation; phase shift; phase response curve; single unit; electrophysiology; glutamate; tetrodotoxin; AP-5; CNQX

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Copyright © 1999 Society for Neuroscience  0270-6474/99/19198630-07$05.00/0

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