ONE PROBABLE MECHANISM OF THE LEARNING-MEMORY DAMAGE BY LEAD:THE CHANGES OF NOS IN HIPPOCAMPUS

Objective To study the effects of lead on the activity and expression of nitric oxide synthase (NOS) and relationship between the effects of lead on learning memory and changes of NOS in subfields of hippocampus. Methods Y maze test was used to study the effects of lead on ability of learning memory; NADPH d histochemistry and immunohistochemistry methods were used to investigate the changes of NOS in subfields of hippocampus. Results Compared with the control group, the ability of learning memory in lead exposed rats was significantly decreased ( P < 0.05 ); the number of NOS positive neurons in CA1 region and dentate gyrus of lead exposed rats was significantly decreased( P < 0.05 ), but no marked changes in CA3 region; the number of nNOS positive neurons in CA1 of lead exposed rats was also significantly decreased( P < 0.05 ), but no obvious changes in CA3. Conclusion Lead could damage the ability of learning memory in rats. Lead could decrease the activity and expression of NOS in hippocampus and had different effects on NOS in different subfields of hippocampus. The changes of NOS in hippocampus induced by lead may be the mechanism of the learning memory damage by lead.

Neuroprotective Effects of Electroacupuncture Preventive Treatment in Senescence-Accelerated Mouse Prone 8 Mice

Objective： To investigate the preventive treatment effects of electroacupuncture（EA） on cognitive changes and brain damage in senescence-accelerated mouse prone 8（SAMP8） mice. Methods： The 5-month-old male SAMP8 and age-matched homologous normal aging mice（SAMR1） were adopted in this study. EA stimulation at Baihui（GV 20） and Yintang（EX-HN 3） was performed every other day for 12 weeks, 4 weeks as a course. Morris water maze test and Nissl-stained with cresyl violet were used for cognitive impairments evaluation and brain morphometric analysis. Amyloid-β（Aβ） expression in hippocampus and parietal cortex was detected by immunohistochemistry, and apoptosis was observed by TUNEL staining. Results： After 3 courses of EA preventive treatment, the escape latencies of 8-month-old SAMP8 mice in EA group were significantly shortened than those of un-pretreated SAMP8 mice. Compared with SAMR1 mice, extensive neuronal changes were visualized in the CA1 area of hippocampus in SAMP8 mice, while these pathological changes and attenuate cell loss in hippocampal CA1 area of SAMP8 mice markedly reduced after EA preventive treatment. Furthermore, Aβ expression in hippocampus and parietal cortex of SAMP8 mice decreased significantly after EA treatment, and neuronal apoptosis decreased as well. Conclusion： EA preventive treatment at GV 20 and EX-HN 3 might improve cognitive deficits and neuropathological changes in SAMP8 mice, which might be, at least in part, due to the effects of reducing brain neuronal damage, decreasing neuronal apoptosis and inhibiting Aβ-containing aggregates.