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In vitro screening methods using cultured Neuro2a cells to examine the activation (phosphorylation) of extracellular signal-regulated kinase (ERK) 1/2 and promotion of neurite outgrowth revealed that the extracts of 5 Kampo (Japanese traditional) formulations have potential as medicines for the treatment of behavioral abnormalities. Since sansoninto (SAT) extract exerted stronger effects than the other candidates tested, we investigated whether its oral administration ameliorates the pathologies of some mouse models of behavioral impairments. The results obtained suggested that SAT extract exerted anti-depression-like effects in the forced swim test, which may be mediated by the up-regulated expression of brain-derived neurotrophic factor (BDNF) in the hippocampus. They may also be mediated by the enhanced phosphorylation of the cAMP response element-binding protein (CREB) via the mitogen-activated protein kinase (MAPK) cascade and Ca/calmodulin-dependent protein kinase II (CaMK II) cascade, a downstream signaling cascade of the N-methyl- d-aspartate (NMDA) receptor. These results indicate that the extract of SAT has potential as a new remedial medicine in the treatment of depression-like behavior. [ABSTRACT FROM AUTHOR]

ABSTRACT Aim Alzheimer's disease ( AD) is associated with a high incidence of sleep disturbance, and several studies have reported that sansoninto ( SNT), a Kampo medicine, ameliorates sleep disturbance. The effects of SNT on sleep disturbance and spatial memory impairment, however, have not been investigated in animal models of AD, therefore the aim of the current study was to carry out these investigations using a rat AD model. Methods Combined cerebral ischemia and intracerebroventricular injections of aggregated beta-amyloid were used to induce a rat model of AD. The quantity and quality of sleep in these rats were determined on electroencephalography and electromyography. Spatial memory impairment was examined using the water maze task. Triazolam, a hypnotic, and donepezil, approved for treating AD, were used as positive controls. Results Compared with sham-operated rats, the AD model rats had decreased total non-rapid eye movement sleep time, more frequent nocturnal awakening in the light phase, and poorer quality of non-rapid eye movement and rapid eye movement sleep on electroencephalography and electromyography. The AD rats also took longer than sham-operated rats to pass the platform area in the water maze retention test. Oral SNT 1000 mg/kg improved those impairments. Conclusion SNT ameliorated not only the abnormal non-rapid eye movement and rapid eye movement sleep structure but also the spatial memory impairment observed in a rat model of AD. [ABSTRACT FROM AUTHOR]