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光敏螯虾神经胶质和神经元细胞超微结构改变的动力学:参与运输过程和神经胶质相互作用的结构。

Dynamics of ultrastructural alterations in photosensitized crayfish glial and neuronal cells: Structures involved in transport processes and neuroglial interactions.

机构信息

Southern Federal University, Rostov-on-Don, Russia.

出版信息

J Neurosci Res. 2011 Mar;89(3):341-51. doi: 10.1002/jnr.22560. Epub 2010 Dec 22.

DOI:10.1002/jnr.22560
PMID:21259321
Abstract

Photodynamic therapy (PDT) is used for cancer treatment, including brain tumors. To explore the dynamics of photodynamic injury of glial cells and neurons and corresponding neuroglial interactions, we studied ultrastructure of the PDT-treated crayfish stretch receptor that consists of a single sensory neuron enwrapped by glial cells. Just after PDT, swelling of some mitochondria, dictyosomes, and endoplasmic reticulum cisterns occurred in neurons and glial cells. Tubular lattices involved in intraglial transport became swollen and disintegrated. At 1 hr postirradiation, these alterations were expanded to the whole cells. Segregation of the neuronal cytoplasm by Nissl bodies, which were involved in protein synthesis and transport along neurites, was lost. Swelling of submembrane cisterns prevented formation of glial protrusions and double-wall vesicles involved in the glia-to-neuron transport. Five hours later, glial layers lost organelles, stuck together, or dilated locally as a result of edema. In the neuronal cytoplasm, only demises of ER and swollen mitochondria were present, but few mitochondria retained normal structure. Thus, swelling of intracellular organelles, the first sign of photodynamic injury, occurred simultaneously in neurons and glia, but glial organelles were eliminated more quickly. Therefore, glial cells were less resistant to PDT than neurons. Adjacent glial layers were damaged less than remote ones, suggesting their protection by the neuron. The structures involved in glia-to-neuron (neuronal submembrane cisterns, glial protrusions, double-wall vesicles), intraglial (tubular lattices), and intraneuronal (Nissl bodies, Golgi apparatus, microtubular bundles) transport were impaired at the earlier stages of stretch receptor damage.

摘要

光动力疗法(PDT)用于癌症治疗,包括脑肿瘤。为了探索神经胶质细胞和神经元的光动力损伤动力学及其相应的神经胶质相互作用,我们研究了由单个感觉神经元被神经胶质细胞包裹组成的螯虾伸展感受器的 PDT 处理后的超微结构。PDT 后即刻,神经元和神经胶质细胞中的一些线粒体、高尔基器和内质网池肿胀。参与神经胶质内运输的管状晶格肿胀并解体。照射后 1 小时,这些改变扩展到整个细胞。参与沿神经突起运输的蛋白质合成和运输的尼氏体将神经元细胞质分隔开的现象消失。亚膜池的肿胀阻止了神经胶质突起和参与神经胶质到神经元运输的双壁小泡的形成。5 小时后,神经胶质层由于水肿而失去细胞器,粘在一起或局部扩张。在神经元细胞质中,只有内质网和肿胀的线粒体死亡,但很少有线粒体保持正常结构。因此,细胞内细胞器的肿胀,即光动力损伤的第一个迹象,同时发生在神经元和神经胶质细胞中,但神经胶质细胞器更快地被消除。因此,神经胶质细胞对 PDT 的抵抗力比神经元低。相邻的神经胶质层比远程的神经胶质层受损小,这表明神经元对其有保护作用。伸展感受器损伤的早期阶段,涉及到神经胶质到神经元(神经元亚膜池、神经胶质突起、双壁小泡)、神经胶质内(管状晶格)和神经元内(尼氏体、高尔基器、微管束)运输的结构受到损害。

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