Objective: Monitoring hemodynamic and vascular changes in the acute stages of mouse stroke models is invaluable in studying ischemic stroke pathophysiology. However, there lacks a tool to simultaneously and dynamically investigate these changes.
Methods: We integrated laser speckle imaging (LSI) and visible-light optical coherence tomography (Vis-OCT) to reveal dynamic vascular responses in acute stages in the distal middle cerebral artery occlusion (dMCAO) model in rodents. LSI provides full-field, real-time imaging to guide Vis-OCT imaging and monitor the dynamic cerebral blood flow (CBF). Vis-OCT offers depth-resolved angiography and oxygen saturation (sO2) measurements.
Results: Our results showed detailed CBF and vasculature changes before, during, and after dMCAO. After dMCAO, we observed insignificant sO2 variation in arteries and arterioles and location-dependent sO2 drop in veins and venules. We observed that higher branch-order veins had larger drops in sO2 at the reperfusion stage after dMCAO.
Conclusion: This work suggests that integrated LSI and Vis-OCT is a promising tool for investigating ischemic stroke in mouse models.
Significance: For the first time, LSI and Vis-OCT are integrated to investigate ischemic strokes in rodent models.
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http://dx.doi.org/10.1109/TBME.2017.2706976 | DOI Listing |
Mol Psychiatry
January 2025
Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA.
Age-related dopamine (DA) neuron loss is a primary feature of Parkinson's disease. However, whether similar biological processes occur during healthy aging, but to a lesser degree, remains unclear. We therefore determined whether midbrain DA neurons degenerate during aging in mice and humans.
View Article and Find Full Text PDFNat Commun
January 2025
Neuroscience Institute, New York University Langone Health, New York, NY, 10016, USA.
Apical and basal dendrites of pyramidal neurons receive anatomically and functionally distinct inputs, implying compartment-level functional diversity during behavior. To test this, we imaged in vivo calcium signals from soma, apical dendrites, and basal dendrites in mouse hippocampal CA3 pyramidal neurons during head-fixed navigation. To capture compartment-specific population dynamics, we developed computational tools to automatically segment dendrites and extract accurate fluorescence traces from densely labeled neurons.
View Article and Find Full Text PDFBiomacromolecules
January 2025
School of Life Science, South China Normal University, Guangzhou 510631, China.
Cerebral ischemic stroke, neuronal death, and inflammation bring difficulties in neuroprotection and rehabilitation. In this study, we developed and designed the ability of natural lactoferrin-polyethylene glycol-polyphenylalanine-baicalein nanomicelles (LF-PEG-PPhe-Bai) to target and reduce these pathological processes, such as neurological damage and cognitive impairment in the stages of poststroke. Nanomicelles made from biocompatible materials have improved bioavailability and targeted distribution to afflicted brain areas.
View Article and Find Full Text PDFStroke
February 2025
Neurovascular Research Unit, Pharmacology Department, Complutense Medical School, Instituto Investigación Hospital 12 Octubre, Madrid, Spain (G.D., B.D., A.M., J.M.P., I.L.).
Background: Acute ischemic stroke treatment typically involves tissue-type plasminogen activator (tPA) or tenecteplase, but about 50% of patients do not achieve successful reperfusion. The causes of tPA resistance, influenced by thrombus composition and timing, are not fully clear. Neutrophil extracellular traps (NETs), associated with poor outcomes and reperfusion resistance, contribute to thrombosis.
View Article and Find Full Text PDFAntioxid Redox Signal
January 2025
Department of Physiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China.
Hypoxia ischemia (HI) is a leading cause of cerebral palsy and long-term neurological sequelae in infants. Given that mitochondrial dysfunction in neurons contributes to HI brain damage, this study aimed to investigate the regulatory role of miR-9-5p in mitochondrial function following HI injury. Overexpression of miR-9-5p in HI mice or HO-exposed PC12 cells suppressed neuronal injury, associated with increased mitochondrial copy number, normalizing mitochondrial membrane potential, improved nuclear factor-erythroid factor 2-related factor 2 (Nrf2) activation, and downregulation of Keap1.
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