POSSIBLE MECHANISM OF RAPID EYE-MOVEMENT SLEEP-DEPRIVATION INDUCED INCREASE IN NA-K ATPASE ACTIVITY

Rapid eye movement sleep deprivation increases Na-K ATPase activity and decreases aminergic neuronal firing rate as well as norepinephrine degrading enzyme, monoamine oxidase, activity. On the other hand, norepinephrine is known to increase Na-K ATPase activity. Hence, this study was conducted to find if the deprivation induced increase in Na-K ATPase activity is mediated by norepinephrine. Rapid eye movement sleep deprived rats were injected with either alpha-1 or beta adrenoceptor antagonist or alpha-2 adrenoceptor agonist and after 8 h the Na-K ATPase activity of the brain was estimated. In an attempt to simulate in vivo conditions, nonrepinephrine was added to an in vitro brain homogenate preparation in the presence or absence of alpha or beta adrenoceptor blockers and the enzyme activity was estimated. The results showed that the enzyme activity was decreased by alpha-1 antagonist as well as by alpha-2 agonist treatment in in vivo preparations. Norepinephrine increased enzyme activity in the in vitro preparation and the increase was prevented by the alpha-1 antagonist. The results of this study suggest that rapid eye movement sleep deprivation induced increase in Na-K ATPase activity may be mediated by norepinephrine acting on either alpha-1 and/or alpha-2 receptors.