Quinpirole, a D2-like Dopaminergic Receptor Agonist, Regulates Neuroinflammation and Reduces NF-κB Nuclear Expression in Microglia from Hippocampus and Brain Cortex Induced by Rapid Eye Movement Sleep Deprivation in Mice

Sleep deprivation is a recognized risk factor for neuroinflammatory and neurodegenerative disorders. Dopamine signaling through D2 receptors (DRD2) has emerged as a potential immunomodulatory pathway in the central nervous system. The present study investigated whether activation of DRD2 by quinpirole (QUIN) modulates astrocytic and microglial responses and NF-κB nuclear translocation in a murine model of rapid eye movement sleep deprivation (RSD). Male CD1 mice were subjected to 72 h of RSD and treated with QUIN (2 mg/kg/day). GFAP, Iba-1, and NF-κB expression were evaluated in hippocampal subregions (CA1, CA3, dentate gyrus) and the medial parietal cortex using immunofluorescence and confocal microscopy. RSD increased GFAP and Iba-1 expression and induced morphological changes consistent with glial activation. Notably, RSD increased NF-κB nuclear expression in microglia. QUIN administration reduced Iba-1 expression, attenuated microglial morphological alterations, and reduced NF-κB nuclear expression across all analyzed regions, even in RSD-subjected mice. These findings suggest that DRD2 activation exerts anti-inflammatory effects in the brain during REM sleep deprivation and that dopaminergic signaling may represent a key target for neuroinflammation associated with sleep loss.