• Applied Microscopy
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• v.36 no.2
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• pp.101-108
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• 2006

Myelin-associated glycoprotein (MAG) has been known to have a crucial role to the formation of myelin sheath during initial stage of myelination. In the present study, we investigated the aging-related expressional changes of MAG in the rat cerebrum. MAG expression was markedly decreased in cerebral cortex by aging. In the adult rat cerebrum, MAG-positive rolls were process-bearing cells with large nucleus, and extensively distributed. However, in the aged rat brain, MAG-positive cells showed small and round morphology with little cytoplasm and few processes. MAG was co-expressed with galatocerebroside, but not with Iba-1, or GFAP. These results suggest that the expressional change of MAG-positive cells is associated with degeneration of oligodendrocyte-myelin system by aging, and that MAG is likely to be a reliable marker for the mature oligodendrocytes in the aged rat brain.

• Applied Microscopy
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• v.36 no.2
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• pp.119-130
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• 2006

To investigate the role of myelin-associated glycoprotein (MAG) in the normal aging process, aging-related morphometric and ultrastructural analyses of the MAG-positive (MAG-(+)) oligodendrocytes were carried out in the cerebral cortex of the Sprague-Dawley rats. In the aged rats, the density of MAG-(+) oligodendrocytes was significantly decreased in the cortical layer (IV-VI) compared with that of the adult rats. However, the percentage of medium and dark types of oligodendrocytes was significantly increased by aging. In the aged rats, the mean nuclear area of the MAG-(-) oligodendrocytes was interestingly reduced compared with that of MAG-(+) oligodendrocytes. In addition, MAG immunoreactive products were markedly decreased in the medium-dark type of oligodendroglial cytoplasm and processes, and were scarcely localized in the dark type of oligodendrocytes of the aged rats. These results suggest that degeneration of oligodendrocytes-myelin system by aging is associated with down regulation of MAG, and that may contribute to further understanding of the biology of MAG in the oligodendrocytes-myelin system.

• Korean Journal of Veterinary Research
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• v.33 no.2
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• pp.295-300
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• 1993

Central nervous system of two dogs with natural canine distemper was investigated histopathologically and immunocytochemically with antisera to MBP, MAG and GFAP. Histopathologically, there were neuronal degeneration and diffuse gliosis in the cerebrum, vacuolar degeneration, hypertrophy of astrocytes and demyelination in cerebellar white matter adjacent to the 4th ventricle and optic tracts showing non-inflammatory demyelinating encephalomyelitis (Summers and Appel, 1987). Immunohistochemically, there was a concurrent disappearance of MBP and MAG in the well developed demyelinating lesion in the cerebellar white matter. At the margin of demyelination, Loss of both MBP and MAG varied on the stage of demyelinating process. GFAP-positive astrocytes were hypertrophied and contained canine distemper virus intranuclear inclusions. GFAP-positive fibers were increased at the early stage of demyelination, and then were not immunoreaeted at the well developed demyelination. Hypertrophic astrocytes with intranuclear inclusions were commonly identified in the interfascular layer without myelin vacuolation and demyelination. This is the first study of primary demyelination and astroglial reactions in natural CDE investigated using immunocytochemistry of two myelin proteins and GFAP. Concurrent loss of MBP and MAG suggest that the myelin sheath is the target in the demyelinating process in CDE.

• The Journal of Korean Physical Therapy
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• v.11 no.3
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• pp.133-140
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• 1999

Why does the CNS not regenerate after injury? The failure of axonal regeneration in the CNS after injury is not due to an inherent inability of these neurons to regrowth axon. Recently, an inhibitory substrate effect of CNS has been discovered which could be directly invoked in the lack of regeneration. The failure of axon regrowth in the CNS is crucially influenced by the presence of neurtie growth inhibitor NI35/250 and possibly also by molecules such as myelin associated glycoprotein(MAG) and chondroitin sulphate proteoglycans(CSPGs). The application of the monoclonal antibody IN-1, which efficinetly neutralizes the N135/250 inhibitory molecules. This new finding has a strong impact on the development of, a new neuroscienctific research directed to stimulate axonal regeneration. In this review summarize the current knowledge on the factors and molecules involved in the regeneration failure.

• Journal of International Academy of Physical Therapy Research
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• v.3 no.1
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• pp.345-355
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• 2012

This study purposed to examine the effect of low power laser on pain response and axonal regeneration. In order to prepare peripheral nerve injury models, we crushed the sciatic nerve of Sprague-Dawley rats and treated them with low power laser for 21 days. The rats were divided into 4 groups: normal group(n=10); control group(n=10) without any treatment after the induction of sciatic nerve crush injury; experimental group I(n=10) treated with low power laser(0.21$mJ/mm^2$) after the induction of sciatic nerve crush injury; and experimental group II(n=10) treated with low power laser(5.25$mJ/mm^2$) after the induction of sciatic nerve crush injury. We measured spontaneous pain behavior(paw withdrawal latency test) and mechanical allodynia(von Frey filament test) for evaluating pain behavioral response, and measured the sciatic function index for evaluating the functional recovery of peripheral nerve before the induction of sciatic nerve crush injury and on day 1, 7, 14 and 21 after the induction. After the experiment was completed, changes in the H & E stain and toluidine blue stain were examined histopathologically, and changes in MAG(myelin associated glycoprotein) and c-fos were examined immunohistologically. According to the results of this study, when low power laser was applied to rat models with sciatic nerve crush injury for 21 days and the results were examined through pain behavior evaluation and neurobehavioral, histopathological and immunohistological analyses, low power laser was found to affect pain response and axonal regeneration in both experimental group I and experimental group II. Moreover, the effect on pain response and axonal regeneration was more positive in experimental group I to which output 0.21$mJ/mm^2$ was applied than in experimental group II to which 5.25$mJ/mm^2$ was applied.