In addition, accumulating clinical evidence has shown that delayed secondary degeneration also occurs in remote non-ischemic cortical regions ( Duering et al., 2015 Wei et al., 2019). Indeed, both clinical studies on stroke patients and animal studies with stroke models reveal the critical role of infarct volume on functional outcome ( Peeling et al., 2001 Roof et al., 2001 Zaidi et al., 2012 Vagal et al., 2015 Turner et al., 2016). Acute neuroprotection to prevent tissue damage within the peri-infarct region and to reduce the final infarct volume is a focus of clinical research ( Majid, 2014). Stroke is one of the leading causes of death and disabilities ( Krishnamurthi et al., 2015) and produces functional deficits resulting from neuronal death in primary lesion areas and from possible secondary degeneration of surrounding or remote regions. At last, we found that primary lesion volume might be the determining factor of motor function deficits. These “direct” fibers mainly represent perilesional, interhemispheric, and subcortical axonal connections. These results suggest that focal ischemic lesions may induce remote WM degeneration, but limited to fibers tied to the primary lesion. Further fiber tractography analysis revealed that only fibers having direct axonal connections with the primary lesion exhibited a significant degeneration. Significant axonal degeneration was observed in the ipsilateral external capsule and even remote regions including the contralesional external capsule and corpus callosum. In this study, we explored the spatial and connectivity properties of white matter (WM) secondary degeneration in a focal unilateral sensorimotor cortical ischemia rat model, using advanced microstructure imaging on a 14 T MRI system. However, the spatial distribution of secondary degeneration along with its role in functional deficits is not well understood. Ischemic lesions could lead to secondary degeneration in remote regions of the brain. 6Zhejiang Provincial Key Laboratory of Cardio-Cerebral Vascular Detection Technology and Medicinal Effectiveness Appraisal, Zhejiang University, Hangzhou, China.5Department of Physical Medicine and Rehabilitation, The Affiliated Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China.4Department of Chemistry, Zhejiang University, Hangzhou, China.3Qiushi Academy for Advanced Studies (QAAS), Zhejiang University, Hangzhou, China.2Key Laboratory of Biomedical Engineering of Education Ministry, College of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, China.1Interdisciplinary Institute of Neuroscience and Technology, School of Medicine, Zhejiang University, Hangzhou, China.On the other hand, the present data do suggest that damage to nervous tissue substantially influences Ca2+ metabolism.Zhaoqing Li 1,2, Huan Gao 2,3, Pingmei Zeng 4, Yinhang Jia 1,5, Xueqian Kong 4, Kedi Xu 2,3,6* and Ruiliang Bai 1,2,5,6* Moreover, it provides no evidence that the several therapeutic treatments that resulted in changes in body fluid Ca2+ also alter cerebral levels of Ca2+. The present study does not support earlier published findings, which suggested that several behaviourally active drugs produce significant decreases of brain Ca2+. Local application of kainic acid and tetrodotoxine to the rat striatum had no acute effects, but kainic acid produced a five to tenfold increase in the levels of striatal Ca2+ 2 weeks after injection. Sleep deprivation for 24 h was ineffective in these experiments. Lithium sulphate produced a small increase of brain Ca2+ 24 h after a high and toxic dose. Cold stress produced a transient increase in the regional levels of Ca2+ in the mouse brain. No major effects with the following drugs, given once or repeatedly to mice at high doses were found: morphine, naloxone, haloperidol, sulpiride, chlordiazepoxide, reserpine, ethanol, mercaptopropionic acid, or pentobarbital. The method is linear (between 1.5 and 5 micrograms Ca2+ ml-1), specific (no other cations present in the brain showed fluorescence) and sensitive (10-100 mg brain tissue can be analyzed). The effects of several drugs and other treatments on the regional levels of Ca2+ in the brain of mice and rats were determined with an automated assay, based on the formation of a fluorescent calcein complex in a continuous flow system.
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