Sleep deprivation induces differential morphological changes in the hippocampus and prefrontal cortex in young and old rats.

Sleep is a fundamental state necessary for maintenance of physical and neurological homeostasis throughout life. Several studies regarding the functions of sleep have been focused on effects of sleep deprivation on synaptic plasticity at a molecular and electrophysiological level, and only a few studies have studied sleep function from a structural perspective. Moreover, during normal aging, sleep architecture displays some changes that could affect normal development in the elderly. In this study, using a Golgi-Cox staining followed by Sholl analysis, we evaluate the effects of 24 h of total sleep deprivation on neuronal morphology of pyramidal neurons from Layer III of the prefrontal cortex (PFC) and the dorsal hippocampal CA1 region from male Wistar rats at two different ages (3 and 22 months). We found no differences in total dendritic length and branching length in both analyzed regions after sleep deprivation. Spine density was reduced in the CA1 of young-adults, and interestingly, sleep deprivation increased spine density in PFC of aged animals. Taken together, our results show that 24 h of total sleep deprivation have different effects on synaptic plasticity and could play a beneficial role in cognition during aging.

Sleep deprivation reduces neuroglobin immunoreactivity in the rat brain.

Neuroglobin (Ngb), a protein located in the mammal's brain, is involved in oxygen transport and free radical scavenging inside the neurons. Ngb colocalizes with choline acetyltransferase in the laterodorsal tegmental nucleus and in the pontine tegmental nucleus, both involved in the sleep-wake cycle regulation. Some studies have shown that free radicals accumulated during prolonged wakefulness are removed during sleep. Therefore, Ngb could act as a regulator of free radicals generated during prolonged wakefulness in the brain. The aim of this study was to determine whether prolonged wakefulness affects Ngb immunoreactivity because of increases in the oxidative stress induced by continuous neuronal activity. For this purpose, male adult Wistar rats were implanted with electrodes for sleep recordings and were divided into control and sleep-deprived groups. Sleep deprivation was carried out for 24 h by gentle handling of the animals. Sleep-wake activity was determined during the deprivation period or 24 h of control conditions. Subsequently, both groups of animals were killed and their brains were obtained and processed for Ngb immunohistochemical analysis and detection of lipid peroxidation. Our data found no evidence of increased oxidative stress in the brains of sleep-deprived animals compared with the controls. The number of Ngb-positive cells was decreased in the sleep-deprived animals in all analyzed areas of the brain compared with the control group. Our results suggest that Ngb could be involved in sleep regulation, independent of its role in the control of oxidative stress.

Sleep-inducing factors.

Kuniomi Ishimori and Henri Piéron were the first researchers to introduce the concept and experimental evidence for a chemical factor that would presumably accumulate in the brain during waking and eventually induce sleep. This substance was named hypnotoxin. Currently, the variety of substances which have been shown to alter sleep includes peptides, cytokines, neurotransmitters and some substances of lipidic nature, many of which are well known for their involvement in other biological activities. In this chapter, we describe the sleep-inducing properties of the vasoactive intestinal peptide, prolactin, adenosine and anandamide.