A novel neurological function of rice bran: a standardized rice bran supplement promotes non‐rapid eye movement sleep in mice through histamine H1 receptors. Issue 11 (29th August 2017) - Um, Min Young
Abstract : Scope: Although rice bran has been shown to be associated with a wide spectrum of health benefits, to date, there are no reports on its effects on sleep. We investigated the effect of rice bran on sleep and the mechanism underlying this effect. Methods and results: Electroencephalography was used to evaluate the effects of standardized rice bran supplement (RBS) and doxepin hydrochloride (DH), a histamine H1 receptor (H1 R) antagonist used as a positive control, on sleep in mice. The mechanism of RBS action was investigated using knockout (KO) mice and ex vivo electrophysiological recordings. Oral administration of RBS and DH significantly decreased sleep latency and increased the amount of non‐rapid eye movement sleep (NREMS) in mice. Similar to DH, RBS fully inhibited H1 R agonist‐induced increase in action potential frequency in tuberomammillary nucleus neurons. In H1 R KO mice, neither RBS nor DH administration led to the increase in NREMS and decrease in sleep latency observed in WT mice. These results indicate that the sleep‐promoting effect of RBS is completely dependent on H1 R antagonism. Conclusions: RBS decreases sleep latency and promotes NREMS through the inhibition of H1 R, suggesting that it could be a promising therapeutic agent for insomnia. Abstract : A standardized rice bran supplement (RBS) and doxepin hydrochloride (DH), a histamine H1 receptor (H1 R) antagonist, significantly decreased sleep latency and increased the amount of non‐rapid eye movement sleep (NREMS) in mice. Like DH, RBS fully inhibited H1 R agonist‐induced increase in action potential frequency in tuberomammillary nucleus neurons. In H1 R KO mice, neither RBS nor DH administration led to the increase in NREMS and decrease in sleep latency observed in WT mice. These results indicate that RBS increases sleep latency and promotes NREMS through the inhibition of H1 R, suggesting that it could be a promising therapeutic agent for insomnia.