The most notable decrease in rapid eye movement (REM) sleep episode count occurs during the light phase, wherein female mice administered with Cabergoline exhibit a reduction of 67.3% in REM sleep episodes (F(1,11)=12.892, P=0.004). Although the most substantial reduction in REM sleep episodes occurs during the dark phase (82.3% fewer REM sleep episodes; F(1,11)=3.667, P=0.082). In male mice, Cabergoline lowers baseline levels of prolactin (PRL) by 98.5% (F(1,6)=13.192, P=0.011), decreasing from 5.8±1.3 to 0.08 ng/mL within 2 hours post-injection. Following a 7-day recovery period, PRL levels revert to values that are statistically indistinguishable from baseline (5.0±0.60 ng/mL; F(1,6)=0.715, P=0.43).

Cabergoline functions as a potent agonist of D2, D3, and 5-HT2B receptors. Pre-exposure to Cabergoline inhibits hydrogen peroxide (H2O2)-induced neuronal cell death in a dose-dependent manner. In the subsequent experiments, a concentration of 10 μM of Cabergoline is employed to explore its neuroprotective effects. Immunostaining for microtubule-associated protein 2 (MAP2) demonstrates that Cabergoline significantly attenuates the neuronal loss induced by H2O2 incubation. The observation of condensed apoptotic nuclei suggests that Cabergoline mitigates apoptotic cell death subsequent to exposure to H2O2.