Increased apoptosis in rat brain after rapid eye movement sleep loss

Abstract

Rapid eye movement (REM) sleep loss impairs several physiological, behavioral and cellular processes; however, the mechanism of action was unknown. To understand the effects of REM sleep deprivation on neuronal damage and apoptosis, studies were conducted using multiple apoptosis markers in control and experimental rat brain neurons located in areas either related to or unrelated to REM sleep regulation. Furthermore, the effects of REM sleep deprivation were also studied on neuronal cytoskeletal proteins, actin and tubulin. It was observed that after REM sleep deprivation a significantly increased number of neurons in the rat brain were positive to apoptotic markers, which however, tended to recover after the rats were allowed to undergo REM sleep; the control rats were not affected. Further, it was also observed that REM sleep deprivation decreased amounts of actin and tubulin in neurons confirming our previous reports of changes in neuronal size and shape after such deprivation. These findings suggest that one of the possible functions of REM sleep is to protect neurons from damage and apoptosis.