Delta power rebound as evidence of sleep need during synthetic torpor in the rat

Periods of natural torpor or hibernation are characterized by markedly reduced metabolic and neural activity, yet animals typically display an intense NREM sleep bout with elevated Delta EEG power immediately upon arousal. This rebound has long been considered an indication that sleep pressure continues to accumulate even during hypometabolic states. However, while some studies support a homeostatic origin of the increase Delta power, others argue that it may simply reflect a non-specific reactivation of cortical networks upon rewarming. A comparable, pronounced Delta increase was also reported in rats, a non-hibernating species, following a pharmacologically induced synthetic torpor. In rats, sleep deprivation following synthetic torpor has also been shown to promote Tau dephosphorylation, suggesting that the physiological events following the return to normothermia may interact with sleep–wake processes. These observations prompted us to assess whether the post–synthetic torpor Delta power increase in this model represents a homeostatic response attributable to sleep loss during the hypometabolic bout. Twelve adult male Sprague–Dawley rats were implanted under general anaesthesia with electrodes for EEG, nuchal and diaphragm EMG recording, a thermistor to measure deep brain temperature, a catheter for arterial pressure recording and heart rate determination; and a microcannula targeting the Raphe Pallidus (RPa). Synthetic torpor was induced by repeated microinjections (100 nl) of the GABA-A receptor agonist muscimol (1 mM) into the RPa, at an ambient temperature of 15 ± 1°C. After six hours of hypothermia, animals were either allowed to recover spontaneously—a condition during which they typically engage in prolonged sleep (n = 6) or kept awake by gentle handling for 6 h (n = 6). Rats subjected to sleep deprivation displayed a robust elevation in NREM sleep Delta power at the beginning of the recovery period (281±13%), which was significantly larger (p < 0.05) than that observed in non-sleep deprived animals (237±19%). The stronger Delta rebound after sleep deprivation supports the hypothesis that the NREM sleep bout which follows synthetic torpor is due to the buildup of a sleep debt during the hypometabolic state. This work was funded by the Italian Ministry of University and Research, and the University of Bologna. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.