Rapid eye movement sleep plays a vital role in the survival of animals. Its deprivation causes alterations in brain functions and behaviors including activities of important enzymes, neurotransmitter levels, impairment of neural excitability and memory consolidation. However, there was a lack of knowledge regarding the effects of rapid eye movement sleep deprivation on neuronal morphology that may get affected much earlier than any permanent damage to the neurons. In the present study, some of these issues have been addressed by studying the effects of rapid eye movement sleep deprivation on various morphological parameters viz. neuronal perimeter, area and shape of neurons located in brain areas known to regulate rapid eye movement sleep and as a control in other brain areas which do not regulate rapid eye movement sleep. The results showed that rapid eye movement sleep deprivation differentially affected neurons depending on their physiological correlates of rapid eye movement sleep and neurotransmitter content. The effects could be reversed if the animals were allowed to recover from rapid eye movement sleep loss or by applying alpha1-adrenergic antagonist, prazosin. The findings in rats support reported data and help explaining previous observations.
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