Tumor necrosis factor-α expression in areas of remote degeneration following middle cerebral artery occlusion of the rat
Section snippets
MCAO
The procedures of the experiments performed in the present study were in accordance with institutional guidelines. All efforts were made to minimize the number of animals and their suffering. For each investigated survival time n=4 animals were killed. Furthermore, three non-operated rats served as controls. In male Sprague–Dawley rats (220–250 g) MCAO was induced by means of the intraluminal suture technique (Longa et al., 1989). Under 2% halothane in 30% oxygen/70% nitrous oxide anesthesia
Glial reaction, TNFα expression and neuronal degeneration within the thalamus
GFAP-immunolabeling of the thalamus of non-operated rats and contralateral to the lesion site revealed a dense network of fiber processes. The GFAP positive cells showed the typical morphology of astrocytes with small cell bodies, the margin of the cytoplasm bearing small rounded edges, and with thin long processes (Fig. 1A). 1 day after MCAO, GFAP positive cells within the thalamus ipsilateral to the lesion site displayed a similar morphology, whereas from 3 days onwards astrocytic cell
Discussion
This is the first paper describing TNFα expression in the substantia nigra and the thalamus following MCAO. These areas displayed no signs of infarction following MCAO; however, selective neuronal damage developed after several days. Similar results have been shown by others Kataoka et al., 1989, Nagasawa and Kogure, 1990, Tamura et al., 1990. The substantia nigra and the thalamus are supplied by the posterior cerebral artery which is not affected by the MCAO technique performed with a 4-0
Acknowledgements
This work has been supported by the START-program, medical faculty of the RWTH Aachen.
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2019, Seminars in Cell and Developmental BiologyCitation Excerpt :Less attention in neuroinflammation has been paid to animal models of remote damage after focal CNS injury. In fact, despite growing number of studies on trauma-induced inflammation at the site of a primary injury and immediately adjacent to this area, few have examined how regions that are remote from the primary injury site also suffer from axonal damage-induced inflammation [37–43]. In general, the remote damage studies have been based on methods that apply axotomy and target deprivation to examine the morphological, biochemical, and ultrastructural changes that occur days to months after injury in brain circuits anatomically and functionally connected to the injury site [44–59].