The present study investigated the neuroprotective effect of γ‐glutamylethylamide (theanine), a component Japanese green tea (Camellia sinensis), on memory impairment induced by twice‐repeated cerebral ischemia in rats. Theanine was injected i.p. immediately after the first occlusion. Theanine (0.3 and 1 mg/kg) significantly prevented the impairment of spatial memory in rats subjected to repeated cerebral ischemia, 7 days after the second reperfusion. Moreover, theanine (1 mg/kg) significantly inhibited the decrease in the number of surviving cells in the hippocampal CA1 field in the same rats. These results suggest that theanine prevents memory impairment induced by repeated cerebral ischemia, in part by protecting against neuronal cell death, and that it might be useful for preventing cerebrovascular disease. Copyright © 2007 John Wiley & Sons, Ltd.

Polychlorinated biphenyls (PCBs) are environmental contaminants that have adverse effects on the endocrine and nervous systems. As they are still detected in breast milk and adipose tissue in humans, the accumulated PCBs may transfer from mothers to children and damage central nervous system. It is revealed from epidemiological studies that cognitive and motor functions were damaged in children born to mothers who ingested PCBs-contaminated foods. However, it remains unclear whether prenatal exposure to PCBs affects emotionality. In the present study, we therefore examined the effect of prenatal exposure to 3,3',4,4',5-pentachlorobiphenyl (PCB126) on emotionality in rats by focusing on anxiogenic behavior and response of the hypothalamus-pituitary-adrenal axis to stress. Pregnant rats were treated orally with PCB126 at a dose of 30 μg/kg or corn oil, its vehicle, on gestational day 15, and their male offspring were subjected to the following experiments at 4-5 weeks old. In an open field test, rats with prenatal exposure to PCB126 showed anxiogenic behavioral responses, including decrease in time spent in the center of an open field and the number of rearings and extension of grooming duration. Interactive behavior, which is an index of anxiety level, was shortened in the social interaction test. The increase in the serum corticosterone level induced by forced swim stress was facilitated by prenatal exposure to PCB126. This evidence suggests that PCB126 may exert anxiogenicity on the offspring of exposed dams, and dysfunction of the hypothalamus-pituitary-adrenal axis may at least in part contribute to this abnormality.

Quantifying the rapid action of a mouse scratching its head with its hind leg can provide an objective behavioral indicator for atopic dermatitis, and the development of new drugs for this disease can be significantly expedited by automating such quantification. In this paper, we propose methods for extracting the scratching patterns of a mouse by focusing on its rapid and periodic behavioral patterns. We extracted the scratching patterns from the high-speed video images of actual laboratory mice, and our experimental results show that scratching can be automatically quantified without misinterpretations. Note to Practitioners - The proposed pattern detection method is completely free from the detection of false behaviors caused by markers painted on their skins. Therefore, practitioners in laboratory experiments can also easily apply it to other periodic behavior analyses, such as gait pattern analysis and tremble detection for automated quantitative evaluations of behaviors related to brain, heart, or other diseases, even if the experimented animals are sensitive to painting.

The present study investigated the effect of schizandrin, a component of the fruit of Schizandra chinesis Baill (Fructus Schizandrae), on memory impairment in rats. Scopolamine (0.5 mg/kg, i.p.), a non‐selective muscarinic receptor antagonist, markedly impaired spatial memory in an eight‐arm radial maze. A higher dose of scopolamine (3 mg/kg, i.p.) also impaired the passive avoidance response. Schizandrin (1 and 10 mg/kg, p.o.) significantly reversed the scopolamine‐induced impairment of spatial memory. Similarly, schizandrin (1 mg/kg, p.o.) significantly reversed the scopolamine‐induced impairment of the passive avoidance response. Moreover, in mice, schizandrin (1 and 10 mg/kg, p.o.) enhanced tremors induced by oxotremorine, a muscarinic M₁ receptor agonist. Taken together these findings suggest that schizandrin reverses scopolamine‐induced memory impairment, in part, by enhancing cholinergic function, and that schizandrin might be useful for treating memory deficits. Copyright © 2007 John Wiley & Sons, Ltd.