Sleep homeostasis in the rat following the induction of a torpor‐like state

Abstract

Soon after the exit from a state of torpor/hibernation, a non‐REM sleep (NREMS) bout with high Delta electroencephalographic activity (EEG) power occurs, suggesting that the time passed in torpor/hibernation is a period of sleep deprivation (Deboer et al., J Comp Physiol A., 1994). The homeostatic nature of the after‐torpor Delta rebound has been challenged (Strijkstra & Daan, Am J Physiol. R, 1998) in the past. According to this alternative view, the Delta enhancement is a consequence of a non‐specific reactivation of cortical activity.We recently found that in the rat, a non‐hibernator, the induction of a torpor‐like state, achieved by multiple injections of muscimol (GABA‐A agonist) into the rostral ventromedial medulla (RVMM), is also followed by a Delta rebound, when the animal recovers from the hypothermic state (Cerri et al., J Neurosci., 2013). The aim of the study was to understand whether the Delta rebound observed in our rats is homeostatically driven or unspecific.We used twelve male Sprague Dawley rats (300–350 g) implanted, under general anaesthesia (Diazepam, 5mg/kg, i.m., Ketamine, 100 mg/kg, i.p.) with: i) electrodes for EEG, and nuchal (nEMG) and diaphragm (dEMG) electromyogram recording, for Wake‐Sleep states scoring; ii) a thermistor for deep brain temperature (Tbrain) recording; iii) a wireless catheter for arterial pressure (AP) and heart rate (HR) recording; iv) a microcannula in the RVMM for drug delivery. Animals were induced into a torpor‐like state by multiple injections of muscimol (1mM, 120 nl) into the RVMM at an ambient temperature (Ta) of 15°C starting at 11 AM. At 5 PM, after 6h of torpor‐like condition, the animals were placed at Ta 28°C in order to favor the rewarming process. After the return to normothermia (8 PM) the animals were either sleep deprived by gentle handling for 6h or left undisturbed (n=6 each).In comparison to their baseline, animals exposed to sleep deprivation showed a powerful increase in Delta power during NREMS soon after the end of the deprivation period. This increase was significantly larger in sleep deprived rats (281±13%) than in non‐deprived animals (237±19%, p<0.05).The size of the Delta rebound in sleep deprived rats indicates that such rebound is not only the consequence of the previous sleep deprivation period, but also of the sleep debt accumulated during the torpor‐like state. Thus, t he Delta rebound which immediately follows a torpor‐like condition is not due to a non‐specific reactivation of cortical activity, but is the expression of a sleep need.