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|Title:||Ultrastructural and immunocytochemical studies of macrophages in an excitotoxin induced lesion in the rat brain||Authors:||Kaur, C.
|Issue Date:||1992||Citation:||Kaur, C., Chan, Y.G., Ling, E.A. (1992). Ultrastructural and immunocytochemical studies of macrophages in an excitotoxin induced lesion in the rat brain. Journal fur Hirnforschung 33 (6) : 645-652. ScholarBank@NUS Repository.||Abstract:||An epidural application of kainic acid (KA) over the cerebral cortex in rat resulted in an extensive lesion in the ipsilateral cerebral cortex. This procedure elicited an accumulation of a large number of macrophages at the site of lesion covering a period of 4 weeks beginning 4 days after the KA application. The macrophages in the centre of lesion were characterized by abundant cytoplasm containing a variable number of lysosomes and phagosomes. Neurons at the same site were depleted during the period examined. They underwent degeneration following the KA treatment. With the monoclonal antibodies OX-42, OX-18 and OX-6, intense immunoreactivity was observed in these cells at the light and electron microscopic levels. Besides these antibodies, the cells were stained positively with the isolectin Griffonia simplicifolia (GSAI-B4). At the periphery of the lesion, many cells bearing the external morphology of microglia were also intensely stained with the GSAI-B4 and the monoclonal antibodies. It was concluded from this study that neuronal degeneration, caused by the excitotoxin KA, induced the accumulation of macrophages which exhibited CR3 receptors (marked by OX-42), MHC I antigen (marked by OX-18) and MHC Ia (marked by OX-6). The expression of these surface antigens may be related to their active phagocytic activity. The reaction with GSAI-B4 indicates the presence of specific lectin receptors on the macrophages which would serve a similar function. The present lectin histochemistry and immunohistochemical studies suggest that macrophages in the centre of the KA-induced lesion were derived from infiltrated monocytes while those at the periphery originated from the activation of local microglial cells.||Source Title:||Journal fur Hirnforschung||URI:||http://scholarbank.nus.edu.sg/handle/10635/131851||ISSN:||00218359|
|Appears in Collections:||Staff Publications|
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