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|Title:||Macrophages/microglia as 'sensors' of injury in the pineal gland of rats following a non-penetrative blast||Authors:||Kaur, C.
|Issue Date:||1997||Citation:||Kaur, C., Ling, E.A., Singh, J., Lim, M.K., Ng, B.L. (1997). Macrophages/microglia as 'sensors' of injury in the pineal gland of rats following a non-penetrative blast. Neuroscience Research 27 (4) : 317-322. ScholarBank@NUS Repository. https://doi.org/10.1016/S0168-0102(97)01164-4||Abstract:||The pineal gland of adult rats was examined immunohistochemically and electron microscopically following exposure of the animals to a single blast equivalent to 110 kg TNT explosive. The most dramatic feature in rats killed at 7, 14 and 21 days after the blast was the upsurge of a large number of macrophages/microglia intensely immunostained with OX-42, OX-18, OX-6 and ED1 antibodies. These antibodies recognise the complement type three (CR3) receptors, major histocompatibility complex class I and class II (MHC I and MHC II) antigens and monocyte/macrophage antigens. Cell counts in OX-42 immunostained sections showed a two-fold increase at these intervals but returned to normal values at 28 days. The immunolabelled cells appeared extremely hypertrophic after the blast when compared with those in normal rats. In the latter and in rats killed at 28 days after the blast, immunoreactive cells were sparsely distributed. Ultrastructural study confirmed a wider occurrence of perivascular macrophages/microglia after the blast and the cells were laden with massive amounts of phagosomes resembling degenerating pinealocyte processes. It is concluded that the seemingly quiescent macrophages/microglia present normally in pineal gland were activated by the external blast force. The induced changes including the increase in cell numbers and endocytosis, however, were reversible in longer surviving animals.||Source Title:||Neuroscience Research||URI:||http://scholarbank.nus.edu.sg/handle/10635/33528||ISSN:||01680102||DOI:||10.1016/S0168-0102(97)01164-4|
|Appears in Collections:||Staff Publications|
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