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The noradrenaline (NA) level in the brain is reduced during rapid eye movement sleep (REMS). However, upon REMS deprivation (REMSD) its level is elevated, which induces apoptosis and the degeneration of neurons in the brain. In contrast, isolated studies have reported that NA possesses an anti-oxidant property, while REMSD reduces lipid peroxidation (LP) and reactive oxygen species (ROS). We argued that an optimum level of NA is likely to play a physiologically beneficial role. To resolve the contradiction and for a better understanding of the role of NA in the brain, we estimated LP and ROS levels in synaptosomes prepared from the brains of control and REMS deprived rats with or without  in vivo  treatment with either α1-adrenoceptor (AR) antagonist, prazosin (PRZ) or α2-AR agonist, clonidine (CLN). REMSD significantly reduced LP and ROS in synaptosomes; while the effect on LP was ameliorated by both PRZ and CLN; ROS was prevented by CLN only. Thereafter, we evaluated  in vitro  the effects of NA, vitamin E (Vit E), vitamin C (Vit C), and desferrioxamine (DFX, iron chelator) in modulating hydrogen peroxide (H 2 O 2 )-induced LP and ROS in rat brain synaptosomes, Neuro2a, and C6 cells. We observed that NA prevented ROS generation by chelating iron (inhibiting a  Fenton  reaction). Also, interestingly, a lower dose of NA protected the neurons and glia, while a higher dose damaged the neurons and glia. These  in vitro  and  in vivo  results are complementary and support our contention. Based on the findings, we propose that REMS maintains an optimum level of NA in the brain (an antioxidant compromised organ) to protect the latter from continuous oxidative onslaught.

frontiers in molecular neuroscience

Noradrenaline Acting on Alpha1 Adrenoceptor as well as by Chelating Iron Reduces Oxidative Burden on the Brain: Implications With Rapid Eye Movement Sleep