In most studies regarding the improving or therapeutical effects induced by enriched environment (EE), EE was performed after the stress treatment or in patients with certain diseases. In the current study, the effects of chronic restraint stress (6 h/day) in mice living in an enriched environment or standard environment (SE) were tested. Mice were randomly divided into 4 groups: non-stressed or stressed mice housed in SE or EE conditions (SE, stress + SE, EE, stress + EE). Prepulse inhibition (PPI) of startle was tested after the 2 weeks or 4 weeks stress and/or EE treatment and 1 or 2 weeks withdrawal from the 4 weeks treatment. After the 4 weeks treatment, spatial recognition memory in Y-maze was also tested. The results showed that EE increased PPI in stressed and non-stressed mice after 2 weeks treatment. No effect of EE on PPI was found after the 4 weeks treatment. 4 weeks chronic restraint stress increased PPI in mice housed in standard but not EE conditions. Stressed mice showed deficits on the 1 h delay version of the Y-maze which could be prevented by living in an enriched environment. Our results indicated that living in an enriched environment reversed the impairing effects of chronic restraint stress on spatial recognition memory. However, EE did not change the effects of stress on PPI.We tested anxiety-like and depression-like behaviors in thansgenic Cnga2–/Y mice. Our results showed that like the olfactory-bulbectomized (OBX) rats, Cnga2–/Y thansgenic mice were anxiety and depressive. They spent less time in the center area of the open field, the time spent in the white box of the white/black box was less in Cnga2–/Y mice than widetype mice. Furthermore, Cnga2–/Y mice were more immobile in forced swim test. After chronic fluoxetine (18mg/kg) treatment, the depressive and anxiety-like behaviour were not ameliated in Cnga2–/Y mice. In conclusion, Cnga2–/Y mice were more anxiety and depressive compared with the widetype mice, but the depression-like behaviour could not be reversed by chronic SSRI treatment. The mechanism under the depression and anxiety-like behaviour in these mice need further studies. Newly encoded memory traces could be reactivated in the hippocampus during slow wave sleep (SWS), and this reactivation is critical for the redistribution and integration of newly encoded memories into the network of preexisting long-term memories. Secondly, the studies during my postgraduate perioid were reported. In this section, one method was introduced, which was a combination of the odor cue related morphine addiction model and a technique for sleep recording in freely moving rats. We trained rats in a conditioned place preference (CPP) paradigm to make the rats associate odor cues (rose or mint) with morphine. EEG was recorded for 3 hr after the training each day. Slow oscillation, spindle and sharp wave ripple events and there durations were analysized from the EEG datas. After the rats learned the association between odor and morphine, morphine related odor or other odors were gave during the sleep to test if morphine related odor would induce memory reactivation and prompt the memory.
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