In contrast, the melatonin monotherapy did not modify the levels of this hormone in the brain tissue, nor the number of neuronal progenitors BrdU/nestin in the group of luzindole + melatonin + REMSD. The beneficial effects of melatonin might be mediated through MT1/MT2 receptors, because this neuroindole exerts its effects by modifying the mitochondrial homeostasis maintenance and preventing the expression of apoptotic genes [65,73,74].
Our findings indicate that REMSD decreases significantly the melatonin levels in the hippocampal tissue.
Our data indicate that exogenous administration of melatonin restores the tissue levels of this hormone in the hippocampus and increases the number of neural precursors and reveals a neuroprotective effect of melatonin against the deleterious consequences of REMSD. The beneficial effects of melatonin on SGZ precursors may rely on its capacity to increase the levels of phospho-c-Raf and phosphoextracellular signal-regulated kinase 1/2 (ERK1/2) through melatonin receptor .
Besides, the behavioral or cognitive consequences of melatonin treatment in REMSD conditions remain to be elucidated.
These effects are observed when melatonin is administered before and during REMSD. Interestingly, melatonin promotes an increase in the tissue levels of Bcl-2 and Bcl-xL of sleep-deprived animals.
Caption: Figure 2: Hippocampal melatonin under REMSD. Bars express means [+ or -] standard deviation.
(*) Statistical differences were found for the control group versus MEL + REMSD and REMSD versus MEL + REMSD groups (** P < 0.021).
BrdU and nestin expression in the subgranular zone of dentate gyrus (DG) of the sleep-deprived group (REMSD) and the MEL + REMSD group.