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作 者:陈翠云[1] 朱慧[1] 李鹏[1] 孙庆艳[1] 华田苗[1]
机构地区:[1]安徽师范大学生命科学学院,安徽芜湖241000
出 处:《解剖学报》2014年第3期304-309,共6页Acta Anatomica Sinica
基 金:国家自然科学基金资助项目(31171082);安徽省教育厅重点资助项目(KJ2009A167);安徽省自然科学基金资助项目(070413138)
摘 要:目的探讨节制饮食对猫初级视皮层内抑制性神经递质γ-氨基丁酸(GABA)和脑源性神经营养因子(BDNF)表达的影响。方法 Nissl染色示初级视皮层分层并用于神经元计数;免疫组织化学方法标记6只猫GABA和BDNF免疫阳性神经元。切片于Olympus光学显微镜下观察摄片,用Image-Pro Express 6.0软件进行细胞计数和免疫阳性反应的吸光度值统计。结果与正常饮食对照猫相比,节制饮食组猫的初级视皮层神经元平均密度无显著变化,GABA免疫阳性神经元密度显著增大,阳性反应的平均吸光度值显著升高;BDNF免疫阳性细胞的密度和阳性反应的平均吸光度值亦明显增大。结论节制饮食能显著增强猫视皮层内GABA和BDNF的表达,这可能对视皮层神经元的结构和功能有保护作用,从而延缓衰老进程。Objective To explore the effect of DR on the expression of inhibitory neurotransmitter ,γ-aminobutyric acid ( GABA) and brain derived neurotrophic factor ( BDNF) in the primary visual cortex of young cats .Methods Totally 6 cats were wsed in this study . Nissl staining was used for cortical layer identification and cell counting . Immunohistochemical techniques were utilized to label GABA-and BDNF-positive neurons .Sections were observed under an Olympus light microscope and photographed with a digital camera .The cell density and absorbance of immunoreactivity were measured with Image-Pro Express 6.0 softwares .Results Our results showed that the mean density of Nissl-stained neurons in the primary visual cortex ( V1) of the DR group showed no significant difference from that of the control group . However , the mean density of GABA-immunoreactive neurons in each cortical layer of V 1 in DR cats was significantly higher than that in control cats .The mean immunoreactive intensity of GABA-positive neurons , as indicated by the average absorbance , increased significantly in DR cats relative to control ones . Accompanied with the elevation of GABA expression, DR enhanced BDNF expression in V1, as indicated by an increased mean density of BDNF-positive neurons and BDNF-immunoreactive average absorbance in DR cats relative to controls .Conclusion These results indicate that dietary restriction leads to a concurrent expression upregulation of GABA and BDNF , which may likely compensate for brain functional degradation during senescence and thus delay aging process .
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