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Administration of Alpha(s1)-Casein Hydrolysate Increases Sleep and Modulates GABA(A) Receptor Subunit Expression
Biomolecules & Therapeutics ; : 268-273, 2018.
Artículo en Inglés | WPRIM | ID: wpr-714740
ABSTRACT
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.
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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Trastornos del Sueño-Vigilia / Vigilia / Caseínas / Salud Mental / Receptores de GABA-A / Enfermedades Neurodegenerativas / Electroencefalografía / Hipotálamo / Neuronas Límite: Animales Idioma: Inglés Revista: Biomolecules & Therapeutics Año: 2018 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Trastornos del Sueño-Vigilia / Vigilia / Caseínas / Salud Mental / Receptores de GABA-A / Enfermedades Neurodegenerativas / Electroencefalografía / Hipotálamo / Neuronas Límite: Animales Idioma: Inglés Revista: Biomolecules & Therapeutics Año: 2018 Tipo del documento: Artículo