Concurrent registration of EEG responses, catecholamine uptake and trypan blue staining in chemical blood-brain-barrier damage

1969 ◽  
Vol 12 (1) ◽  
pp. 16-22 ◽  
Author(s):  
S. Flodmark ◽  
A. Hamberger ◽  
B. Hamberger ◽  
O. Steinwall
Keyword(s):  
Blood Brain Barrier ◽  
Trypan Blue ◽  
Brain Barrier ◽  
Blue Staining ◽  
Trypan Blue Staining ◽  
Catecholamine Uptake ◽  
Blood Brain ◽  
Blood Brain Barrier Damage

scholarly journals Severe Hypoglycemia Contributing to Cognitive Dysfunction in Diabetic Mice is Associated with Pericyte and Blood–Brain Barrier Dysfunction

2021 ◽  
Author(s):  
Lu Lin ◽  
Lishan Huang ◽  
Lijing Wang ◽  
Yubin Wu ◽  
Zhou Chen ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Cognitive Dysfunction ◽  
Blood Brain Barrier ◽  
Severe Hypoglycemia ◽  
Brain Barrier ◽  
Blue Staining ◽  
Diabetic Patients ◽  
Inflammatory Factor ◽  
Diabetic Mice ◽  
Blood Brain

Abstract Background: Severe hypoglycemia can cause cognitive impairment in diabetic patients, but the underlying molecular mechanism remains unclear.Objective: To assess the effect of severe hypoglycemia on cognitive function in diabetic mice to clarify the relationship between the mechanism and dysfunction of pericytes and the blood–brain barrier (BBB).Method: We established type 1 diabetes mellitus in 80 male C57BL/6J mice by intraperitoneal injection of streptozotocin (180 mg/kg). Further abdominal injection of short-acting insulin induced severe hypoglycemia. The mice were divided into normal, diabetes, and diabetic + severe hypoglycemia groups, and their blood glucose and general weight index were examined. Pericyte and BBB morphology and function were detected by histological and western blot analyses, BBB permeability was detected by Evans blue staining, and cognitive function was detected with the Morris water maze.Results: Severe hypoglycemia aggravated the histological damage, BBB damage, brain edema, and pericyte loss in the diabetic mice. It also reduced the expression of the BBB tight junction proteins occludin and claudin-5, the expression of the pericyte-specific markers PDGFR-β (platelet-derived growth factor receptor-β) and α-SMA, and increased the expression of the inflammatory factor MMP9. At the same time, diabetic mice with severe hypoglycemia had significantly reduced cognitive function.Conclusion: Severe hypoglycemia leads to cognitive dysfunction in diabetic mice, and its possible mechanism is related to pericyte dysfunction and BBB destruction.

Angiopoietin-like protein 1 decreases blood brain barrier damage and edema following focal cerebral ischemia in mice

2008 ◽  
Vol 52 (3) ◽  
pp. 470-477 ◽  
Author(s):  
Dar-Ming Lai ◽  
Hung Li ◽  
Chin-Cheng Lee ◽  
Yi-Shiuan Tzeng ◽  
Yu-Hsuan Hsieh ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Blood Brain Barrier ◽  
Focal Cerebral Ischemia ◽  
Brain Barrier ◽  
Blood Brain ◽  
Blood Brain Barrier Damage

Potential of immunoglobuline treatment in motor neuron diseases associated to blood-brain barrier damage

2021 ◽  
Vol 429 ◽  
pp. 119406
Author(s):  
Lucrezia Becattini ◽  
Francesca Bianchi ◽  
Alessandra Govoni ◽  
Erika Schirinzi ◽  
Andrea Bacci ◽  
...  
Keyword(s):  
Motor Neuron ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Motor Neuron Diseases ◽  
Blood Brain ◽  
Blood Brain Barrier Damage

scholarly journals PET-MRI nanoparticles imaging of blood–brain barrier damage and modulation after stroke reperfusion

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Justine Debatisse ◽  
Omer Faruk Eker ◽  
Océane Wateau ◽  
Tae-Hee Cho ◽  
Marlène Wiart ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Ischaemic Stroke ◽  
Blood Brain Barrier ◽  
Acute Ischaemic Stroke ◽  
Brain Parenchyma ◽  
Brain Barrier ◽  
Resonance Imaging ◽  
Blood Brain ◽  
Blood Brain Barrier Damage

Abstract In an acute ischaemic stroke, understanding the dynamics of blood–brain barrier injury is of particular importance for the prevention of symptomatic haemorrhagic transformation. However, the available techniques assessing blood–brain barrier permeability are not quantitative and are little used in the context of acute reperfusion therapy. Nanoparticles cross the healthy or impaired blood–brain barrier through combined passive and active processes. Imaging and quantifying their transfer rate could better characterize blood–brain barrier damage and refine the delivery of neuroprotective agents. We previously developed an original endovascular stroke model of acute ischaemic stroke treated by mechanical thrombectomy followed by positron emission tomography-magnetic resonance imaging. Cerebral capillary permeability was quantified for two molecule sizes: small clinical gadolinium Gd-DOTA (<1 nm) and AGuIX® nanoparticles (∼5 nm) used for brain theranostics. On dynamic contrast-enhanced magnetic resonance imaging, the baseline transfer constant Ktrans was 0.94 [0.48, 1.72] and 0.16 [0.08, 0.33] ×10−3 min−1, respectively, in the normal brain parenchyma, consistent with their respective sizes, and 1.90 [1.23, 3.95] and 2.86 [1.39, 4.52] ×10−3 min−1 in choroid plexus, confirming higher permeability than brain parenchyma. At early reperfusion, Ktrans for both Gd-DOTA and AGuIX® nanoparticles was significantly higher within the ischaemic area compared to the contralateral hemisphere; 2.23 [1.17, 4.13] and 0.82 [0.46, 1.87] ×10−3 min−1 for Gd-DOTA and AGuIX® nanoparticles, respectively. With AGuIX® nanoparticles, Ktrans also increased within the ischaemic growth areas, suggesting added value for AGuIX®. Finally, Ktrans was significantly lower in both the lesion and the choroid plexus in a drug-treated group (ciclosporin A, n = 7) compared to placebo (n = 5). Ktrans quantification with AGuIX® nanoparticles can monitor early blood–brain barrier damage and treatment effect in ischaemic stroke after reperfusion.

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