Acute sleep deprivation induces synaptic remodeling at the soleus muscle neuromuscular junction in rats.

Sleep is important for cognitive and physical performance. Sleep deprivation not only affects neural functions but also results in muscular fatigue. A good night's sleep reverses these functional derangements caused by sleep deprivation. The role of sleep in brain function has been extensively studied. However, its role in neuromuscular junction (NMJ) or skeletal muscle morphology is sparsely addressed although skeletal muscle atonia and suspended thermoregulation during rapid eye movement sleep possibly provide a conducive environment for the muscle to rest and repair; somewhat similar to slow-wave sleep for synaptic downscaling. In the present study, we have investigated the effect of 24 h sleep deprivation on the NMJ morphology and neurochemistry using electron microscopy and immunohistochemistry in the rat soleus muscle. Acute sleep deprivation altered synaptic ultra-structure viz. mitochondria, synaptic vesicle, synaptic proteins, basal lamina, and junctional folds needed for neuromuscular transmission. Further acute sleep deprivation showed the depletion of the neurotransmitter acetylcholine and the overactivity of its degrading enzyme acetylcholine esterase at the NMJ. The impact of sleep deprivation on synaptic homeostasis in the brain has been extensively reported recently. The present evidence from our studies shows new information on the role of sleep on the NMJ homeostasis and its functioning.

Acute sleep deprivation elevates brain and body temperature in rats.

Available sleep deprivation studies lack data on simultaneous changes in hypothalamic, cortical and body temperature during sleep deprivation and recovery. Ten adult male Wistar rats chronically implanted with electroencephalogram, electro-oculogram and electromyogram electrodes for recording sleep were used in this study. Hypothalamic and cortical temperatures were measured by pre-implanted thermocouples. A radio transmitter (TA10TAF-40, DSI USA) was implanted intraperitoneally to measure body temperature. All the temperatures were measured simultaneously at 15-s intervals during baseline conditions, sleep deprivation and recovery sleep. Sleep deprivation was carried out for 24 hr by the gentle handling method; however, sleep and temperature were only recorded during the first 12 hr of deprivation. During sleep deprivation the body, hypothalamic and cortical temperatures increased significantly as compared to baseline. During recovery sleep, body and cortical temperature recovered earlier than the hypothalamic temperature. Hypothalamic temperature remained higher than the baseline values throughout 12 hr of recovery sleep. In the recovery sleep, cortical temperature decreased immediately and reached near baseline by 4 hr. We observed a quicker return of cortical temperature towards control temperature during recovery sleep compared with hypothalamic and body temperature. The results of the present study show that acute sleep deprivation results in a rise in both cortical and hypothalamic temperature, along with body temperature. A rise in cortical temperature may be a contributing factor for cognitive dysfunction resulting from sleep deprivation.

Cortex senses environmental temperature earlier than the hypothalamus in awake rats.

Simultaneous and direct recording of temperature from the body, hypothalamus, and cortex in animals exposed to acute thermal challenges lack evidence. This study was conducted to assess the usual concept, that brain temperature is rather stable when animals are exposed to different ambient temperatures. In this study, we report the characteristic changes in the body, hypothalamic, and cortical temperature, when the rats were acutely exposed to cold (6 °C) and hot (36 °C) ambient temperature. The results of our study show that the body temperature is robustly regulated while hypothalamic and cortical temperatures vary on challenges to ambient cold (6 °C) and warm (36 °C) exposure in awake rats. The onset of response was observed quickest in the cortex, indicating that the cortical thermal sensing may relay intracranial thermal input to the hypothalamus for the regulation of body temperature within narrow limits. The present findings contradict earlier evidence, which stated that the brain does not participate in thermal sensing.