| Summary: | 碩士 === 國立陽明大學 === 解剖暨細胞生物學研究所 === 89 === ABSTRACT
Methamphetamine (MAP) is an illicit drug and has been abused worldwide. High dose MAP cause severe neurotoxic effect. The neurotoxic effect may involve the overloading of oxidative stress followed by creating cell death-related genes. Deprenyl, an irreversible inhibitor of monoamine oxidase B, has been used to treat Parkinson’s disease and Alzheimer’s disease because of its neuroprotective effect, especially of its antiapoptosis and immunoenhancement. The goals of these experiments were to test whether deprenyl can have neuroprotective effect against high-dose MAP-induced toxicity. Male Sprague-Dawley rats (250-350g) were randomly assigned into four groups: 1) MAP; 2) MAP+Deprenyl; 3)Deprenyl; 4) Saline. In MAP group, MAP(5mg/kg, i.p.) were given 4 times consecutively at 2 hr interval. In MAP+Deprenyl group, the antiapoptotic dose of deprenyl(0.25mg/kg, i.p.) were given 1hr after MAP for the 1st day, and then once daily for 3 weeks or 8 weeks, depends on the group assigned. The 14C-2-deoxyglucose method were used to evaluate the Local Cerebral Glucose Utilization (LCGU) of the 28 cognitive brain regions for each groups. The results showed that high-dose MAP cause significant decrease(p<0.05) in the LCGUs of all of the 28 regions read in MAP group, and that in MAP+Deprenyl group, the deprenyl treatment, both in 3-week’s and 8-week’s, did cause the MAP-reduced LCGUs returned back to the value of Saline-control group. The two-way ANOVA results also showed that there are significant interaction (p<0.05) between the MAP and the deprenyl and indicated that deprenyl did have neuroprotective effect against high-dose MAP-induced toxicity.
In conclusion, our results suggested that high dose MAP cause significant LCGUs decrease in all of 28 cognitive brain regions read. These regions include neocortex, limbic system, basal ganglia. Further, low-dose deprenyl effectively rescued the decreased LCGUs caused by the high-dose MAP neurotoxicity .
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