Hibernation has been proposed as a tool for human space travel. In recent years, a procedure to induce a metabolic state known as “synthetic torpor” in non-hibernating mammals was successfully developed. Synthetic torpor may not only be an efficient method to spare resources and reduce psychological problems in long-term exploratory-class missions, but may also represent a countermeasure against cosmic rays. Here we show the preliminary results from an experiment in rats exposed to ionizing radiation in normothermic conditions or synthetic torpor. Animals were irradiated with 3 Gy X-rays and organs were collected 4 h after exposure. Histological analysis of liver and testicle showed a reduced toxicity in animals irradiated in torpor compared to controls irradiated at normal temperature and metabolic activity. The expression of ataxia telangiectasia mutated (ATM) in the liver was significantly downregulated in the group of animal in synthetic torpor. In the testicle, more genes involved in the DNA damage signaling were downregulated during synthetic torpor. These data show for the first time that synthetic torpor is a radioprotector in non-hibernators, similarly to natural torpor in hibernating animals. Synthetic torpor can be an effective strategy to protect humans during long term space exploration of the solar system.

Tau is a key protein in neurons, where it affects the dynamics of the microtubule system. The hyperphosphorylation of Tau (PP-Tau) commonly leads to the formation of neurofibrillary tangles, as it occurs in tauopathies, a group of neurodegenerative diseases, including Alzheimer's. Hypothermia-related accumulation of PP-Tau has been described in hibernators and during synthetic torpor (ST), a torpor-like condition that has been induced in rats, a non-hibernating species. Remarkably, in ST PP-Tau is reversible and Tau de-phosphorylates within a few hours following the torpor bout, apparently not evolving into pathology. These observations have been limited to the brain, but in animal models of tauopathies, PP-Tau accumulation also appears to occur in the spinal cord (SpCo). The aim of the present work was to assess whether ST leads to PP-Tau accumulation in the SpCo and whether this process is reversible. Immunofluorescence (IF) for AT8 (to assess PP-Tau) and Tau-1 (non-phosphorylated Tau) was carried out on SpCo coronal sections. AT8-IF was clearly expressed in the dorsal horns (DH) during ST, while in the ventral horns (VH) no staining was observed. The AT8-IF completely disappeared after 6 h from the return to euthermia. Tau-1-IF disappeared in both DH and VH during ST, returning to normal levels during recovery. To shed light on the cellular process underlying the PP-Tau pattern observed, the inhibited form of the glycogen-synthase kinase 3β (the main kinase acting on Tau) was assessed using IF: VH (i.e., in motor neurons) were highly stained mainly during ST, while in DH there was no staining. Since tauopathies are also related to neuroinflammation, microglia activation was also assessed through morphometric analyses, but no ST-induced microglia activation was found in the SpCo. Taken together, the present results show that, in the DH of SpCo, ST induces a reversible accumulation of PP-Tau. Since during ST there is no motor activity, the lack of AT8-IF in VH may result from an activity-related process at a cellular level. Thus, ST demonstrates a newly-described physiological mechanism that is able to resolve the accumulation of PP-Tau and apparently avoid the neurodegenerative outcome.

Tau protein is of primary importance for neuronal homeostasis and when hyperphosphorylated (PP-Tau), it tends to aggregate in neurofibrillary tangles, as is the case with tauopathies, a class of neurodegenerative disorders. Reversible PP-Tau accumulation occurs in the brain of hibernating rodents and it was recently observed in rats (a non-hibernator) during synthetic torpor (ST), a pharmacological-induced torpor-like condition. To date, the expression of PP-Tau in the rat enteric nervous system (ENS) is still unknown. The present study immunohistochemically investigates the PP-Tau expression in the myenteric plexus of the ileum and colon of normothermic rats (CTRL) and during ST, focusing on the two major subclasses of enteric neurons, i.e., cholinergic and nitrergic.Results showed that both groups of rats expressed PP-Tau, with a significantly increased percentage of PP-Tau immunoreactive (IR) neurons in ST vs. CTRL. In all rats, the majority of PP-Tau-IR neurons were cholinergic. In ST rats, the percentage of PP-Tau-IR neurons expressing a nitrergic phenotype increased, although with no significant differences between groups. In addition, the ileum of ST rats showed a significant decrease in the percentage of nitrergic neurons. In conclusion, our findings suggest an adaptive response of ENS to very low core body temperatures, with changes involving PP-tau expression in enteric neurons, especially the ileal nitrergic subpopulation. In addition, the high presence of PP-Tau in cholinergic neurons, specifically, is very interesting and deserves further investigation. Altogether, these data strengthen the hypothesis of a common cellular mechanism triggered by ST, natural hibernation and tauopathies occurring in ENS neurons.

Small mammals exhibit seasonal changes in intestinal morphology and function via increased intestine size and resorptive surface and/or nutrient transport capacity to increase energy yield from food during winter. This study investigated whether seasonal or acute acclimation to anticipated or actual energetic challenges in Djungarian hamsters also resulted in higher nutrient resorption capacities due to changes in small intestine histology and physiology. The hamsters show numerous seasonal energy saving adjustments in response to short photoperiod. As spontaneous daily torpor represents one of these adjustments related to food quality and quantity, it was hypothesized that the hamsters’ variable torpor expression patterns are influenced by their individual nutrient uptake capacity. Hamsters under short photoperiod showed longer small intestines and higher mucosal electrogenic transport capacities for glucose relative to body mass. Similar observations were made in hamsters under long photoperiod and food restriction. However, this acute energetic challenge caused a stronger increase of glucose transport capacity. Apart from that, neither fasting-induced torpor in food-restricted hamsters nor spontaneous daily torpor in short photoperiod-exposed hamsters clearly correlated with mucosal glucose transport capacity.Both seasonally anticipated and acute energetic challenges caused adjustments in the hamsters’ small intestine. Short photoperiod appeared to induce an integration of these and other acclimation processes in relation to body mass to achieve a long-term adjustment of energy balance. Food restriction seemed to result in a more flexible, short-term strategy of maximizing energy uptake possibly via mucosal glucose transport and reducing energy consumption via torpor expression as emergency response.

Rats are highly social animals that are able to emit audible sounds, but mainly intercommunicate in an ultrasonic interval of frequency (Brudzynski, ILAR journal, 2009). Adult rats emit ultrasonic vocalizations in two different frequencies, 22KHz and 50KHz. Vocalizations at 22KHz are mostly used in situations with negative connotations and are used as warning and alert signals, while those emitted at 50 Hz express hedonic states (Brudzynski, Curr Opin Neurobiol, 2013). In an attempt to obtain a detailed evaluation of the animal behaviour in a study regarding sleep and obesity, we recorded the emission of vocalizations at 22Hz as monitor of the animals well being. Unexpectedly, we found vocalizations during REM sleep. Thus, we quantitatively analyzed this behavior, in an attempt to unravel its functional significance. 15 Sprague‐Dawley male rats, adapted to a standard Light‐Dark (LD) cycle of 12h‐12h (L: 09:00–21:00), were administered for eight weeks with a normocaloric diet (NC, n=7), or hypercaloric (35% of fat) (IC, n=8), with subsequent obesity development. Under general anaesthesia, animals were implanted with: i) electrodes for electroencephalography (EEG), and nuchal (nEMG) and diaphragmatic electromyography (dEMG); ii) a catheter in the femoral artery for telemetric arterial pressure recording; iii) a hypothalamic thermistor. After recovery from surgery, animals’ parameters in basal conditions were recorded for two consecutive days. The sound emission was recorded by means of a “Bat Detector” ‐‐‐‐(BatBox III D) set for acquisition at 22KHz. Similarly to what observed in the wake state, during REM sleep the vocalization occurs during what appears to be a prolonged expiratory event (diaphragmatic contraction). The event can manifest as a single, or, more often, in ‘series’ that appear during the subsequent ‘expiratory’ events. Thus, for each animal, separating L(resting), and D (active) phases, the following parameters were evaluated: a) number of series/hour of REM sleep; b) series duration, calculated as time from the beginning of the first event and the end of the last event every series; c) mean number of events for each series. A preliminary analysis shows that vocal series appear with similar probability (No./h of REM sleep) in lean and obese animals, both in the L and D phase (NCL=2.8±0.7; NCD=1.8±0.6; ICL=2.6±1; ICD=2.6±0.7). Similar results can also be observed for the series duration (NCL=7.2±1.2s; NCD=6.4±2.5s; ICL=8.4±3s; ICD=8.8±1.8s) and the mean number of events for each series (NCL=2.8±0.3; NCD=3.0±1.7; ICL=2.0±0.5; ICD=2.7±0.6). The statistical analysis (two‐way ANOVA for repeated measures), showed no significant effects induced by the LD cycle or the animals weight. The appearance of ultrasonic vocalizations during REM sleep is not affected by either the LD ciclicity or the animal weight, supporting the hypothesis that these events represent a REM sleep constitutive phenomenon rather than being the consequence of a respiratory pathophysiological process.