内生大麻素受体激动剂抑制异动症大鼠纹状体单胺类神经递质的释放

目的观察内生大麻素受体激动剂WIN 55,212-2对帕金森病左旋多巴相关异动症模型大鼠纹状体内单胺类神经递质释放的影响。方法采用脑内微透析和高效液相色谱在线递质测量法观察WIN 55,212-2腹腔内注射对异动症模型大鼠左旋多巴相关异动症状和纹状体内单胺类神经递质释放的影响。结果与溶剂注射相比,WIN 55,212-2注射显著抑制异动症模型大鼠左旋多巴皮下注射后的异动样症状(F1 263=44.071,P<0.001),同时明显减少纹状体内多巴胺的释放(F1 263=5.091,P<0.05)。结论纹状体内生大麻素受体可能通过抑制性的调节单胺类神经递质的释放来影响异动症模型大鼠的异动样症状。     

Correlative factors of cognitive impairment in patients with lacunar infarcts I.

Objective To study the relationships between cognitive impairment in patients with lacunar infarcts and quantitative CT measures and to determine the independent correlative factors of cognitive impairment. Methods Neuropsychological examination was conducted for 128 patients with acute lacunar infarct. Number, location, and volume of infarcts, cerebral atrophy index and severity of white matter lesions （WMLs） were measured and recorded. Results The number of lacunar infarcts in cognitive impairment （CI） group was significantly larger than that in cognitive normal （CN） group. Mean width of sulcns and sylvian fissure, index of frontal horn and ventricular-brain ratio （VBR） were significantly different in both groups. There were more patients with 3 grades or 4 grades WMLs in CI group （62%） than those in CN group （22%）. The total volume of lacunar infarcts showed no statistically significant difference. Logistic regression analysis indicated that the number of lacunar infarcts in frontal subcortex and thalamus, the volume of infarcts in anterior periventricular white matter, width of cerebral sulcns and sylvian fissure were correlated with cognitive impairment respectively. Additionally, age and education were correlative factors of cognitive impairment in patients with lacunar infarct. Conclusion Correlative factors of cognitive impairment in patients with lacunar infarct are not merely one feature, but a combination of infarct features （number, location, and volume）, cortical atrophy and host factors （age and education）.     

Correlative factors of cognitive impairment in patients with lacunar infarcts

Patients with lacunar infarcts are thought tohave an increased risk of cognitive i mpair ment anddementia[1].Cognitive i mpair ment is a predictor ofpoor functional outcome in stroke survivors[2].However,in patients with lacunar infarcts,thepathway leading to cognitive i mpair ment is notclear.According to the lacunar hypothesis,cogni-tive i mpair ment results fromincreased number andvolume of lacunes,especially whenlocated strategi-cally within frontal subcortical loops[3];while Feinet al[4]f…