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