Cerebral ischemia causes cell death of vulnerable neurons in mammalian brain. Wistar adult rats (male and female, weighing 180-280 g) were submitted to 2 min, 10 min, or to 2 and 10 min (separated by a 24-h interval) of transient forebrain ischemia by the four-vessel occlusion method. Animals subjected to the longer ischemic episodes had massive necrosis of pyramidal CA1 cells of the hippocampus, while animals receiving double ischemia (2 + 10 min) showed neuronal tolerance to the ischemic insult. ATP-diphosphohydrolase activity from hippocampal synaptosomes was assayed in these three groups (N = 6 animals/group) under two conditions: no reperfusion and 5-min of reperfusion. The control values for ATPase and ADPase activities were 144.7 +/- 18.8 and 60.6 +/- 5.24 nmol Pi min-1 mg protein-1, respectively. The 10-min group without reperfusion showed an enhancement of approximately 20% for ATPase and ADPase activities. In reperfused rats, only the 2-min group had a 20% increase in both enzymatic activities. We suggest that modulation of ATP-diphosphohydrolase activity might be involved in molecular events that follow both ischemia and reperfusion.
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CNS Neurosci Ther
January 2025
Beijing Key Laboratory of Hypoxia Translational Medicine, Xuanwu Hospital, Center of Stroke, Beijing Institute of Brain Disorder, Capital Medical University, Beijing, China.
Objective: Ischemia-reperfusion of the abdominal aorta often results in damage to distant organs, such as the heart and brain. This cellular heterogeneity within affected tissues complicates the roles of specific cell subsets in abdominal aorta occlusion model (AAO) injury. However, cell type-specific molecular pathology in the hippocampus after ischemia is poorly understood.
View Article and Find Full Text PDFInt J Dev Neurosci
February 2025
Department of Digestive and Nutrition, College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China.
Neonatal hypoxic-ischemic encephalopathy (HIE) is a severe neurological injury during infancy, often resulting in long-term cognitive deficits. This study aimed to investigate the neuroprotective effects of Edaravone (EDA), a free radical scavenger, and elucidate the potential role of brain-derived neurotrophic factor (BDNF) in mediating these effects in neonatal HIE rats. Using the Rice-Vannucci model, HIE was induced in neonatal rats, followed by immediate administration of EDA after the hypoxic-ischemic insult.
View Article and Find Full Text PDFJ Am Heart Assoc
January 2025
Background: Left ventricular (LV) geometric patterns are associated with cognitive impairment and cerebral small vessel disease. As a novel magnetic resonance imaging marker of cerebral small vessel disease and a risk factor for cognitive dysfunction, cortical cerebral microinfarcts (CMIs) have been associated with heart disease through mechanisms including cardioembolism and cerebral hypoperfusion. Further investigation is required to determine whether cortical CMIs could arise from hemodynamic changes related to LV geometry, thus elucidating the connection between LV geometry and cognitive function.
View Article and Find Full Text PDFActa Neurochir (Wien)
January 2025
Department of Neurosurgery, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, 226014, Uttar Pradesh, India.
Background: Reaching parenchymal segments of the lateral lenticulostriate artery (LSA) perforators, which represent the medial resection limit in insular gliomas (IG), remains a challenge. The currently described methods are indirect and sometimes, imprecise.
Methods: We report an antegrade direct skeletonization technique to identify these tiny arteries at the medial end of IGs with an illustrative case of grade 2 astrocytoma.
Sci Data
January 2025
Hubei Clinical Research Center of Central Nervous System Repair and Functional Reconstruction, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, 442000, China.
Ischemic stroke constitutes a multifaceted neurological affliction that spans various cellular types. Lack of dynamic chromatin accessibility data after stroke is one of the obstacles to understanding this process. To gain insights into the variations in transcriptional regulation among various cell types subsequent to a stroke, we employed single-nucleus ATAC-seq to curate a chromatin accessibility compendium from the cerebral cortex of mice subjected to middle cerebral artery occlusion/reperfusion (MCAO/R).
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