RT Journal Article SR Electronic T1 Circadian Rhythms in the Suprachiasmatic Nucleus are Temperature-Compensated and Phase-Shifted by Heat Pulses In Vitro JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 8630 OP 8636 DO 10.1523/JNEUROSCI.19-19-08630.1999 VO 19 IS 19 A1 Ruby, Norman F. A1 Burns, D. Erik A1 Heller, H. Craig YR 1999 UL http://www.jneurosci.org/content/19/19/8630.abstract AB 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°Cin vitro. Rhythm period was 23.9 ± 0.1 and 23.7 ± 0.1 hr at 37 and 31°C, respectively; the Q10for 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.