Sleep is the most basic and essential physiological requirement for mental health, and sleep disorders pose potential risks of metabolic and neurodegenerative diseases. Tryptic hydrolysate of α(S1)-casein (α(S1)-CH) has been shown to possess stress relieving and sleep promoting effects. However, the differential effects of α(S1)-CH on electroencephalographic wave patterns and its effects on the protein levels of γ-aminobutyric acid A (GABA(A)) receptor subtypes in hypothalamic neurons are not well understood. We found α(S1)-CH (120, 240 mg/kg) increased sleep duration in mice and reduced sleep-wake cycle numbers in rats. While α(S1)-CH (300 mg/kg) increased total sleeping time in rats, it significantly decreased wakefulness. In addition, electroencephalographic theta (θ) power densities were increased whereas alpha (α) power densities were decreased by α(S1)-CH (300 mg/kg) during sleep-wake cycles. Furthermore, protein expressions of GABA(A) receptor β1 subtypes were elevated in rat hypothalamus by α(S1)-CH. These results suggest α(S1)-CH, through GABA(A) receptor modulation, might be useful for treating sleep disorders.
Animals ; Caseins* ; Electroencephalography ; Hypothalamus ; Mental Health ; Mice ; Neurodegenerative Diseases ; Neurons ; Rats ; Receptors, GABA-A* ; Sleep Wake Disorders ; Wakefulness