• 대한수의학회지
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• 제38권2호
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• pp.290-296
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• 1998

Histological changes was investigated in the 4 weeks old rat brain using NMDA (N-methyl-D-asparate) which is capable of mediating excitotoxic events. The changes were occured when the injected NMDA solved in PBS was over $1.0{\mu}g/g$(about 90nM). The necrosis of Purkinje cells in cerebellum and the increasement of coloidal plexus cell number were prevalent. The Purkinje cell number of necrosis were increased according to increasement of amount of injected NMDA. In spite of increasement of degenerated Purkinje cell number, differentiation of new Purkinje cell was not identified because total number of Purkinje cell was not changed. The change of cell number was observed in coloidal plexus cell rather than degeneration of cell. About 5 time increasement was occured. This change may cause increasement of cerebrospinal fluid and the makes mophorogy of brain more round than nomal.

• Molecules and Cells
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• 제20권2호
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• pp.219-227
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• 2005

Purkinje cell degeneration (pcd) mice are characterized by death of virtually all cerebellar Purkinje cells by postnatal day 30. In this study, we used DNA microarray analysis to investigate differences in gene expression between the brains of wild type and pcd mice on postnatal day 20, before the appearance of clear-cut phenotypic abnormalities. We identified 300 differentially expressed genes, most of which were involved in metabolic and physiological processes. Among the differentially expressed genes were several calcium binding proteins including calbindin-28k, paravalbumin, matrix gamma-carboxyglutamate protein and synaptotagamins 1 and 13, suggesting the involvement of abnormal $Ca^{2+}$ signaling in the pcd phenotype.

• 생물정신의학
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• 제7권2호
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• pp.164-173
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• 2000

This study was carried out to investigate the direct neurotoxicity of alcohol on CNS and the effects of piracetam or vitamins on ultrastructural changes of the rat cerebellar and hippocampal neurons during long-term alcohol treatment. To evaluate the results, quantitative analysis were done for light and electronic microscopic findings. On the light microscopy, red degeneration of pyramidal cells and Purkinje cells was found more apparently in the alcohol only treated group than in the control group. On the electron microscopy, increased lipofuscin pigments were found in cerebellum and hippocampus. In quantitative analysis, vitamins significantly reduced red degeneration in both hippocampus and cerebellum. However, piracetam significantly reduced red degeneration in cerebellum but not in hippocampus. Lipofuscin pigments in Purkinje cells and pyramidal cells were significantly reduced in the alcohol with piracetam treated group than the alcohol only treated group. However, vitamins had no significant reducing effect of lipofuscin pigments in Purkinje cells and pyramidal cells. According to the results, it is concluded that vitamins deficiency might cause red degeneration of pyramidal cell after long-term alcohol treatment, but increment of lipofuscin pigments in pyramidal and Purkinje cell may be caused by alcohol itself or its metabolite rather than vitamins deficiency. Piracetam seems to improve cognitive function impairment caused by alcohol consumption.

• 대한임상검사과학회지
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• 제47권1호
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• pp.51-58
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• 2015

Ethanol has long been implicated in triggering apoptotic neurodegeneration. Alcohol also may indirectly harm the fetus by imparing the mother's physiology. We examined the effects of ethanol on immature brain of mice. Three-weeks-old female ICR strain mice daily intraperitoneally injected with ethanol at the concentration of 4 and 20% in saline for 0, 6, and 24 hours and 1 and 4 weeks. The mice were weighted and sacrificed, and the brains were ectomized for the present histological, immunohistochemical and TUNEL assays. Based on the histologic hematoxylin and eosin stain, immunohistochemical expression of glutamate receptor protein and neuronal cell adhesion molecule (NCAM) were evaluated. The cerebral cortex of the ethanol-treated group showed few typical symptoms of apoptosis such as chromosome condensation and disintegration of the cell bodies. TUNEL staining revealed DNA fragmentation in the 6 and 24 hours. This results demonstrated that acute ethanol administration causes neuronal cell death. I found that either glutamate receptor inhibition or activation could induce cerebellar degeneration as ethanol effect. Neuronal death also can be induced by excess activity of certain neurotransmitter, including glutamate. Neurons must establish cell-to-cell contact during growth and development in order to survive, migrate to their final destination, and develop appropriate connections with neighboring cell. Purkinje cell in cerebellar are especially vulnerable to the cell death and degeneration. After ethanol treatment in cerebellar, NCAM had decreased by 4 weeks. This result suggest that apoptosis seems to be involved in the slow elimination of neuron and cerebellar degeneration.

• The Korean Journal of Physiology and Pharmacology
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• 제13권5호
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• pp.373-378
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• 2009

Cerebellar Purkinje cells (PCs) play a crucial role in motor functions and their progressive degeneration is closely associated with spinocerebellar ataxias. Although immunohistochemical (IHC) analysis can provide a valuable tool for understanding the pathophysiology of PC disorders, the method validation of IHC analysis with cerebellar tissue specimens is unclear. Here we present an optimized and validated IHC method using antibodies to calbindin D28k, a specific PC marker in the cerebellum. To achieve the desired sensitivity, specificity, and reproducibility, we modified IHC analysis procedures for cerebellar tissues. We found that the sensitivity of staining varies depending on the commercial source of primary antibody. In addition, we showed that a biotin-free signal amplification method using a horseradish peroxidase polymer-conjugated secondary antibody increases both the sensitivity and specificity of ICH analysis. Furthermore, we demonstrated that dye filtration using a $0.22\;{\mu}m$ filter eliminates or minimizes nonspecific staining while preserving the analytical sensitivity. These results suggest that our protocol can be adapted for future investigations aiming to understand the pathophysiology of cerebellar PC disorders and to evaluate the efficacy of therapeutic strategies for treating' these diseases.

• Applied Microscopy
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• 제35권3호
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• pp.165-176
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• 2005

소뇌의 버그만아교세포는 인접한 조롱박신경세포를 둘러싸는 특이한 해부학적 분포를 하고 있어 종래로부터 조롱박신경세포에 대한 물리적 지지 역할과 함께 이 신경 세포의 생존과 기능에 필요한 대사물질을 공급해 주는 것으로 추정되어 왔으나 이에 대한 구체적인 연구는 많지 않다. 본 연구에서는 버그만아교세포와 조롱박신경세포의 상관관계를 증명하기 위한 연구로 전자현미경적 정상적인 미세구조와 신경독물인 하르말린을 흰쥐에 투여하여 조롱박신경세포만을 특이적으로 파괴시킨 소뇌조직을 대상으로 최근 버그만아교세포에서 발현되는 것으로 알려진 수 종의 대사성 단백물질의 동향을 면역조직 화학방법으로 관찰하여 GLAST의 면역 염색성은 정상부위보다 신경세포 손상부위의 버그만아교세포에서 현저히 감소되었다. 하르말린 투여군의 흰쥐에서 조롱박신경세포의 사멸은 소뇌벌레에서 집중적으로 일어났으며 사멸된 부위는 calbindin D-28K에 염색된 정상 조롱박신경세포들 사이에서 산발적으로 끼어 있는 빈 공간으로 나타났는데 빈공간은 분자층과 조롱박신경세포층이 세로로 달리는 좁고 긴 띠 (bands) 모양의 특이 한 양상을 보였다. MT 면역염색성은 신경세포 손상부위의 버그만아교세포에서 현저히 증가하였다. 이상의 관찰 결과로 볼 때 조롱박신경세포의 손상에 의하여 버그만아교세포는 강한 아교세포반응을 보이며 MT의 발현을 통하여 인접 신경세포 손상과 미세아교세포 활성에 의하여 유발된 산화성 스스로를 보호하고 생존한다. 그러나 GLAST의 발현의 감소는 조롱박신경세포의 사멸로 인하여 이들 세포들로부터 유리되어 나오는 글루타메이트의 감소 또는 중단되므로 버그만아교세포에서 이들 글루타메이트 수송체 역할이 감소되었음을 반영하는 것으로 사료된다.93({\pm}0.053){\mu}m$ 였다. 으뜸세포의 사립체의 크기는 정상대조군, 종양대조군 및 BCG 투여군이 각각 $0.80({\pm}0.130){\mu}m,\;0.83({\pm}0.143){\mu}m$ 및 $0.72({\pm}0.078){\mu}m$ 였다. 이상의 결과를 종합해보면 BCG를 반복 투여하면 위점막으뜸세포의 분비과립이 약간 작아지는 등 분비기능이 다소 억제되나 그 정도가 경미하여 으뜸세포의 분비기능에 큰 손상을 주지 않는 것으로 생각된다.모양을 비교한 결과 꼬리핵과 줄무늬체바닥핵에서는 모두 가지돌기가시(dendritic spine)에 연접하였으나, 중격옆핵과 중격핵에서는 가지돌기 (dendrite)에 연접하는 것과 가지돌기가시에 연접하는 것이 혼재하였다. 이들 두 신경핵 무리는 이마앞겉질에서 기원하는 축삭종말의 연접차이로 볼 때 서로 다른 회로계통에 속할 것으로 생각되며, 문헌고찰을 통해서 꼬리핵과 줄무늬체바닥핵은 줄무늬체회로 (striatal circuit)에 속하고 중격옆핵과 중격핵은 변연계통회로(limbic circuit)에 속할 것으로 판정했다. 이마앞겉질은 생리적, 약리적, 신경학적 및 형태학적 근거들로 보아 바닥핵들을 통해 변연계통과 대뇌겉질 전체에 영향을 미칠 것으로 여겨지는데, 본 실험에서는 네 종류의 바닥핵들, 즉 꼬리핵, 줄무늬체바닥핵, 중격옆핵 및 중격핵과 관련된 신경연접들을 관찰하였으며, 그 결과를 문헌 고찰한 결과 변연계통과 줄무늬체계통이 앞뇌의 바닥에 있는 신경핵들에서 형태학적 교차연결을 통해 정서와 마음의 상태를 행동과 대응으로 표현하는 중요한 신경회로가 존재함을 제안하였다.腎臟組織)에서 더많이 발생되었다.

• 국제물리치료학회지
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• 제1권2호
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• pp.91-98
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• 2010

This study is intended to examine the motor skill learning and treadmill exercise on motor performance and synaptic plasticity in the cerebellar injured rats by harmaline. Experiment groups were divided into four groups and assigned 15 rats to each group. Group I was a normal control group(induced by saline); Group II was a experimental control group(cerebellar injured by harmaline); Group III was a group of motor skill learning after cerebellar injured by harmaline; Group IV was a group of treadmill exercise after cerebellar injured by harmaline. In motor performance test, the outcome of group II was significantly lower than the group III, IV(especially group III)(p<.001). In histological finding, the experimental groups were destroy of dendrities and nucleus of cerebellar neurons. Group III, IV were decreased in degeneration of cerebellar neurons(especially group III). In immunohistochemistric response of synaptophysin in cerebellar cortex, experimental groups were decreased than group I. Group III's expression of synaptophysin was more increased than group II, IV. In electron microscopy finding, the experimental groups were degenerated of Purkinje cell. These result suggest that improved motor performance by motor skill learning after harmaline induced is associated with dynamically altered expression of synaptophysin in cerebellar cortex and that is related with synaptic plasticity.

• 대한물리의학회지
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• 제5권3호
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• pp.455-465
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• 2010

Purpose : This study is intended to examine the motor skill learning on balance and coordination in the cerebellar injured rats by 3AP. Methods : This study selected 60 Sprague-Dawley rats of 8 weeks. Experiment groups were divided into four groups and assigned 15 rats to each group. Group I was a normal control group(induced by saline); Group II was a experimental control group(cerebellar injured by 3AP); Group III was a group of motor skill learning after cerebellar injured by 3AP; Group IV was a group of treadmill exercise after cerebellar injured by 3AP. In each group, motor performance test, histologic observations, synaptophysin expression and electron microscopy observation were analyzed. Results : In motor performance test, the outcome of group II was significantly lower than the group III, IV(especially group III)(p<.001). In histological finding, the experimental groups were destroy of dendrities and nucleus of cerebellar neurons. Group III, IV were decreased in degeneration of cerebellar neurons(especially group III). In immunohistochemistric response of synaptophysin in cerebellar cortex, experimental groups were decreased than group I. Group III's expression of synaptophysin was more increased than group II, IV. In electron microscopy finding, the experimental groups were degenerated of Purkinje cell. Conclusion : These result suggest that improved motor performance by motor skill learning after harmaline induced is associated with dynamically altered expression of synaptophysin in cerebellar cortex and that is related with synaptic plasticity.

• 한국임상수의학회지
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• 제11권1호
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• pp.485-505
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• 1994

고양이에서 납중독에 따른 육안적 조직병리학적 변화를 밝히고 납투여 용량과 조직남종도와의 관계를 규명하기 위하여 42마리의 고양이를 대상으로 체중에 따라 0(대조군), 10, 100(저용량), 1000, 2000, 4000(고용량)ppm의 lead acetate를 경구적으로 투여하여 납독성을 평가하였다. 준임상형 납중독에서 흡수된 납의 80% 이상이 뼈에 침착되었다. 반면에 심급성 납중독에서 흡수된 납의 42%가 뼈에, 36%와 20%가 신장과 간장에 각각 침착되었다. 간장은 황갈색조를 보였고 신경계에는 육안적 병변이 관찰되지 않았다. 가장 두드러진 조직병리학적 소견은 대뇌에 신경원괴사였다. 한마리의 고용량 투여 고양이에서 성상세포 증식이 관찰되었다. 6마리에 고용량투여 고양이의 대뇌피질에서 신경교증이 관찰되었다. 2마리의 고용량 투여 고양이 대뇌 피질 회백질에서 가장 깊은 층에 수초탈락이 있었고 혈관주위에 적혈구의 유출과 공동화가 한마리의 고용량 투여 고양이의 대뇌에서 관찰되었다. 6마리의 고용량투여 고양이에서 소뇌의 Purkinje cell의 변성을 보였다. 말초신경의 현미경적 소견은 분명하지 않았다. 심급성 중독에서 7마리의 고양이의 신장 근위곡세뇨관 상피세포와 5마리 고양이의 간장 간세포에 납봉입체가 관찰되었다. 이들 봉입체는 H&E 염색에서 볼 수 있으며 orcein 염색에서 더 잘 관찰된다. 2 마리의 고용량 투여 고양이에서 신장의 세뇨관간에 공포화와 결합조직 증식이 있었다. 22마리의 고양이 간장에 문맥주위 간세포의 공동화가 관찰되었다. 5마리의 처치 고양이 고환에 정세관의 공포화와 정조 포수의 감소가 관찰되었다. 3마리의 고용량 투여 고양이에 난소낭종이 있었으며 2마리의 고양이에서 난자발생이 좋지 않았다. 고양이에서 납중독은 조직병리학적 변화에 근거하여 의심할 수 있고 이 소견들은 진단에 도움이 된다. 또한 사후 조직내 납분석은 납중독 진단에 도움이 된다.