Circadian rhythms in the suprachiasmatic nucleus are temperature-compensated and phase-shifted by heat pulses in vitro

Temperature compensation and the effects of heat pulses on rhythm phase wer e assessed in the suprachiasmatic nucleus (SCN). Circadian neuronal rhythms were recorded from the rat SCN at 37 and 31 degrees C in vitro. Rhythm per iod was 23.9 +/- 0.1 and 23.7 +/- 0.1 hr at 37 and 31 degrees C, respective ly; the Q(10) for tau was 0.99. Heat pulses were administered at various ci rcadian times (CTs) by increasing SCN temperature from 34 to 37 degrees C f or 2 hr. Phase delays and advances were observed during early and late subj ective night, respectively, and no phase shifts were obtained during midsub jective 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 mu M)] and non -NMDA [CNQX (10 mu M)] receptor antagonists or by tetrodotoxin (TTX) at con centrations of 1 or 3 mu M. The phase response curve for heat pulses is sim ilar to ones obtained with light pulses for behavioral rhythms. These data demonstrate that circadian pacemaker period in the rat SCN is temperature-c ompensated over a physiological range of temperatures. Phase delays were no t caused by activation of ionotropic glutamate receptors, release of other neurotransmitters, or temperature-dependent increases in metabolism associa ted with action potentials. Heat pulses may have phase-shifted rhythms by d irectly altering transcriptional or translational events in SCN pacemaker c ells.