Zhang Jing, Ma Jing, Wang Guang-Fa
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2014 Mar;30(2):153-6.
To observe the changes of mitochondria stress in locus coeruleus and the tyrosine hydroxylasic projection after long-term sleep deprivation.
Sleep deprivation mice model was set up by employing "novel environments" method. The expression of NAD -dependent deacetylase Sirtuin type 3 (SIRT3), which regulates mitochondrial energy production and oxidative stress, and heat shock protein 60 (HSP60), a major biomarker of mitochondrial stress, and the tyrosine hydroxylasic projection from locus coeruleus were analyzed after a 5-day sleep deprivation.
Compared to the control group, the expression of SIRT3 in locus coeruleus was significantly decreased in respouse to long-term sleep deprivation, while the expression of HSP60 was significantly increased. In addition, relative to control group, pereentage area of the tyrosine hydroxylasic projection to anterior cingulate cortex was substantial decreased in long-term sleep deprivation group.
Long-term sleep deprivation induced the decreased level of SIRT3 expression and the elevation of mitochondrial stress in locus coenileus, which may further lead to the loss of tyrosine hydroxylasic projection in mice.
观察长期睡眠剥夺后蓝斑及酪氨酸羟化酶投射区的线粒体应激变化。
采用“新环境”法建立睡眠剥夺小鼠模型。在睡眠剥夺5天后，分析调节线粒体能量产生和氧化应激的烟酰胺腺嘌呤二核苷酸依赖的Ⅲ型组蛋白去乙酰化酶（SIRT3）、线粒体应激的主要生物标志物热休克蛋白60（HSP60）的表达，以及蓝斑的酪氨酸羟化酶投射。
与对照组相比，长期睡眠剥夺后蓝斑中SIRT3的表达显著降低，而HSP60的表达显著增加。此外，相对于对照组，长期睡眠剥夺组中酪氨酸羟化酶投射至前扣带回皮质的面积百分比大幅降低。
长期睡眠剥夺导致蓝斑中SIRT3表达水平降低和线粒体应激升高，这可能进一步导致小鼠酪氨酸羟化酶投射丧失。
