Abstract
White matter tract (WMT) degeneration has been reported to occur following a stroke, and it is associated with post-stroke functional disturbances. White matter pathology has been suggested to be an independent predictor of post-stroke recovery. However, the factors that influence WMT remodeling are poorly understood. Cortisol is a steroid hormone released in response to prolonged stress, and elevated levels of cortisol have been reported to interfere with brain recovery. The objective of this study was to investigate the influence of corticosterone (CORT; the rodent equivalent of cortisol) on WMT structure post-stroke. Photothrombotic stroke (or sham surgery) was induced in 8-week-old male C57BL/6 mice. At 72 h, mice were exposed to standard drinking water ± CORT (100 µg/mL). After two weeks of CORT administration, mice were euthanised and brain tissue collected for histological and biochemical analysis of WMT (particularly the corpus callosum and corticospinal tract). CORT administration was associated with increased tissue loss within the ipsilateral hemisphere, and modest and inconsistent WMT reorganization. Further, a structural and molecular analysis of the WMT components suggested that CORT exerted effects over axons and glial cells. Our findings highlight that CORT at stress-like levels can moderately influence the reorganization and microstructure of WMT post-stroke.
Highlights
White matter tract (WMT) integrity post-stroke is an area of significant interest, as it is a parameter that correlates with long-term recovery potential [1]
Wallerian degeneration is characterised by the progressive degeneration of axons, followed by the infiltration of resident macrophages and infiltrating monocytes, which results in the degradation of myelin and atrophy of the WMTs [4]
We examined white matter loss from two major WMTs, the corpus callosum (CC) and the corticospinal tract (CST)
Summary
White matter tract (WMT) integrity post-stroke is an area of significant interest, as it is a parameter that correlates with long-term recovery potential [1]. WMTs can be directly damaged at the time of stroke, but are affected by secondary Wallerian degeneration [2,3]. The association between stroke and secondary Wallerian degeneration of white matter has 4.0/). Been explored in a number of preclinical [2,5,6,7,8] and clinical studies [9,10]. Neuroimaging studies suggest that these changes are associated with neurological deficits and poorer functional outcomes post-stroke [11,12,13].
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