马里兰大学医学院的研究人员利用珊瑚虫发出光芒的蛋白，点亮了在中枢神经系统中发挥关键作用的脑细胞。这种荧光标记蛋白可帮助科学家了解与多种精神疾病有关的脑细胞缺陷。研究结果刊登于2006年12月20日的Journal of Neuroscience中。
粒线体缺陷可能是阿兹海默症、帕金森氏症以及中风和衰老过程的一个环节。研究人员用这种标记，区别神经元的粒线体与神经胶质细胞的粒线体。
研究小组负责人Krish Chandrasekaran副教授认为，这项新技术可以帮助研究人员解决许多问题，例如引起帕金森氏症和阿兹海默症之神经元粒线体功能缺陷之程度如何，也可以观察神经元粒线体是否会随着年龄增长而发生变化。
研究人员利用先进的遗传工程技术，制造出携带可鉴别神经元粒线体之荧光蛋白的小鼠。他们再利用显微镜观察这些小鼠的大脑，神经元粒线体结构会发出黄绿色光。研究人员已经证实，这些荧光蛋白的表现并不会影响神经元粒线体的正常功能。
荧光标记系统可用来探测神经活动方式、粒线体能量制造系统的调节方式，以及帮助研究人员了解二者间的交互作用。
(资料来源 : Bio.com)
英文原文摘要：
Neuron-Specific Conditional Expression of a Mitochondrially Targeted Fluorescent Protein in Mice
Krish Chandrasekaran, Julie L. Hazelton, Yu Wang, Gary Fiskum, and Tibor Kristian
Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland 21201
Correspondence should be addressed to either Krish Chandrasekaran or Tibor Kristian, Medical School Teaching Facility 5-34, 685 West Baltimore Street, Baltimore, MD 21201. Email: kchan004@umaryland.edu or Email: tkris001@umaryland.edu
Mitochondrial dysfunction contributes to the pathophysiology of both acute and chronic neurodegenerative disorders. Quantification of mitochondrial bioenergetic properties generally requires the use of isolated brain mitochondria. However, the involvement of neuronal mitochondrial dysfunction in these disorders is limited by the lack of markers, and therefore isolation procedures, that distinguish neuronal compared with astrocyte mitochondria. To address this and other issues concerning neuronal mitochondria in the CNS, transgenic mice were generated that express a fluorescent protein targeted specifically to neurons. A neuron-specific promoter, CaMKII (calcium/calmodulin-dependent kinase II) driven tTA (tetracycline transactivator) mice were crossed with TRE (tetracycline responsive element) driven mitochondrial targeted enhanced yellow fluorescent protein (eYFP) mice. Expression of eYFP in the bigenic mouse brain was observed only in neuronal mitochondria of striatum, forebrain, and hippocampus and was enhanced by the removal of the tetracycline analog doxycycline (Dox) in the diet. The respiratory control ratio of synaptic and nonsynaptic mitochondria isolated from eYFP-expressing mice was the same as control mice, suggesting that neuronal mitochondria expressing eYFP maintain normal bioenergetic functions. More importantly, the development of Dox-inducible, neuron targeted mito/eYFP transgenic mice offer a unique in vivo model for delineating the participation of neuronal mitochondria in neuronal survival and death.
Key words: cortex; hippocampus; neuron; mitochondria; transgenic; mice; eYFP; tetracycline; respiration; neurodegeneration; energy metabolism
Received Sept. 25, 2006; revised Nov. 14, 2006; accepted Nov. 14, 2006.
Correspondence should be addressed to either Krish Chandrasekaran or Tibor Kristian, Medical School Teaching Facility 5-34, 685 West Baltimore Street, Baltimore, MD 21201. Email: kchan004@umaryland.edu or Email: tkris001@umaryland.edu
