• Title/Summary/Keyword: Cat retina

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Microglial Reaction to the Cytotoxicity of 5,7-Dihydroxytryptamine in the Cat Retina (5,7-Dihydroxytryptamine의 세포독성에 의한 고양이 망막내 미세아교세포의 반응양상)

  • Joo, Woo-Hyun;Nam, Seong-Ahn;Jo, Seung-Mook;Cho, Hyon-Hoo;Shin, Min-Cheol;Won, Moo-Ho;Choi, Chang-Do
    • Applied Microscopy
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    • v.28 no.4
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    • pp.425-434
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    • 1998
  • This study was designed to investigate the microglial reactions to the neurodegenerative changes in the cat retina. All experiments were performed using adult cats of both sex, weighing $2,500g\sim3,500g$. 5,7-DHT $(100{\mu}g)$ dissolved in 0.1% ascorbic acid was injected into the vitreous body. All injections were performed in one-side eye; the other side served as the control, which was injected only with 0.1% ascorbic acid. Cats were sacrificed at 1, 3, 7, 14 and 21 days after intravitreal injection of 5,7-DHT For light microscopy, retinae were fixed with 4% paraformaldehyde and processed using NDPase histochemistry. Same retinae were fixed with 1% para(formaldehyde-2.5% glutaraldehyde and processed for electron microscopy. NDPase-positive microglial cells were mainly distributed in the inner plexiform layer of the retina, and characterized by a small somata with a few slender processes, which were also extended in the ganglion cell layer (GCL) and inner nuclear layer (INL). The intensity of the microglia stained for NDPase was abruptly increased at 7 day as compared with that of the control, and thereafter continuously sustained until 21 day, the last experimental group in this study. Under the electron microscopical observation, microglial cells in the control group exhibited elongate nucleus with perinuclear chromatin condensation, and the perikaryon was scanty. However, a few hypertrophic glial cells were frequently found at 3 days after the drug injection. By 7 day, most microglial cells directed toward the degenerated neurons in the GCL, and the number of microglial cells was slightly increased as compared with the former group. At the 14 day, most microglial cells wrapped the degenerated cells in the GCL, and a few cells showed phagocytotic features. By 21 day, most microglial cells were engaged in phagocytotic activity, and their cytoplasm was filled with the phagorytosed material. Based on the results, 5,7-DHT may act as a specific neurotoxin to the cat retina, and microglial reactions to the neuronal death are already induced in early experimental stage. These results indicate that the microglial cells in the cat retina show characteristic features as a protective effect of neural tissue.

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Effect of n-3 fatty acid deficiency on fatty acid compositions of nervous system in rats reared by artificial method. (N-3 지방산 결핍이 혈청 및 신경조직의 지방산 조성에 미치는 영향)

  • Lim, Sun-Young
    • Journal of Life Science
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    • v.17 no.5 s.85
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    • pp.634-640
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    • 2007
  • Our previous study suggested that n-3 fatty acid deficiency was associated with significantly reduced spatial learning as assessed by Morris water maze test. Here we investigated an effect of n-3 fatty acid deficiency on rat brain, retina and serum fatty acyl compositions at 15 wks age using a first generational artificial rearing technique. Newborn Rat pups were separated on day 2 and assigned to two artificial rearing groups or a dam-reared control group. Pups were hand fed artificial milk via custom-designed nursing bottles containing either 0.02%(n-3 Deficient) or 3.1% (n-3 Adequate) of total fatty acids as a-linolenic acid(LNA). At day 21, rats were weaned to either n-3 deficient or n-3 adequate pelleted diets and fatty acid compositions of brain, retina and liver were analyzed at 15 wks age. Brain docosahexaenoic acid(DHA) was lower(58% and 61%, P<0.05) in n-3 deficient in comparison to n-3 adequate and dam-reared groups, receptively, while brain docosapentaenoic acid(DPAn-6) was increased in the n-3 deficient group. In retina and serum fatty acid compositions, the decreased precentage of DHA and increased precentage of DPAn-6 were observed. These results suggested that artificial rearing method can be used to produce n-3 fatty acid deficiency in the first generation and that adequate brain DHA levels are required for optimal brain function.