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Relevant bibliographies by topics / Blood-brain barrier Ultrastructure

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Academic literature on the topic 'Blood-brain barrier Ultrastructure'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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Journal articles on the topic "Blood-brain barrier Ultrastructure"

1

Stewart, P. A., K. Hayakawa, and C. L. Farrell. "Quantitation of blood-brain barrier ultrastructure." Microscopy Research and Technique 27, no. 6 (April 15, 1994): 516–27. http://dx.doi.org/10.1002/jemt.1070270606.

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2

STEWART, P. A., C. R. FARRELL, and B. L. COOMBER. "Blood-Brain Barrier Ultrastructure: Beyond Tight Junctions." Annals of the New York Academy of Sciences 529, no. 1 Fourth Colloq (June 1988): 295–97. http://dx.doi.org/10.1111/j.1749-6632.1988.tb51486.x.

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3

Wang, Jinqiao, Chunyan Ma, Jing Zhu, Gaofeng Rao, and Hongjuan Li. "Effect of 3-Aminobenzamide on the Ultrastructure of Astrocytes and Microvessels After Focal Cerebral Ischemia in Rats." Dose-Response 18, no. 1 (January 1, 2020): 155932581990124. http://dx.doi.org/10.1177/1559325819901242.

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The disruption of blood–brain barrier (BBB) is a critical event in the formation of brain edema during early phases of ischemic brain injury. Poly(ADP-ribose) polymerase (PARP) activation, which contributes to BBB damage, has been reported in ischemia–reperfusion and traumatic brain injury. Here, we investigated the effect of 3-aminobenzamide (3-AB), a PARP-1 inhibitor, on the ultrastructure of BBB. Male Sprague Dawley rats were suffered from 90 minutes of middle cerebral artery occlusion, followed by 4.5 hours or 22.5 hours of reperfusion (R). The vehicle or 3-AB (10 mg/kg) was administered intraperitoneally (ip) 60 minutes after lacking of blood. Tissue Evans Blue (EB) levels, ultrastructures of astrocytes and microvessels, and areas of perivascular edema were examined in penumbra and core, at I 1.5 hours /R 4.5 hours and I 1.5 hours /R 22.5 hours, respectively. The severity of ultrastructural changes was graded with a scoring system in each group. We showed that 3-AB treatment significantly decreased tissue EB levels and ultrastructural scores, attenuated damages in astrocytes and microvessels, and reduced areas of perivascular edema. In conclusion, PARP inhibition may provide a novel therapeutic approach to ischemic brain injury.

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4

Garbuzova-Davis, Svitlana, Edward Haller, Samuel Saporta, Irina Kolomey, Santo V. Nicosia, and Paul R. Sanberg. "Ultrastructure of blood–brain barrier and blood–spinal cord barrier in SOD1 mice modeling ALS." Brain Research 1157 (July 2007): 126–37. http://dx.doi.org/10.1016/j.brainres.2007.04.044.

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Nag, Sukriti, and Stephen C. Pang. "Effect of atrial natriuretic factor on blood–brain barrier permeability." Canadian Journal of Physiology and Pharmacology 67, no. 6 (June 1, 1989): 637–40. http://dx.doi.org/10.1139/y89-101.

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Recent studies have demonstrated receptors for atrial natriuretic factor on endothelium of intracerebral vessels. The physiological role of these receptors is not known. The present study was undertaken to determine whether atrial natriuretic factor has an effect on blood–brain barrier permeability to protein and ions using horseradish peroxidase and lanthanum as markers of permeability alterations. This study does not demonstrate a significant effect of atrial natriuretic factor on blood–brain barrier permeability mechanisms in steady states.Key words: blood–brain barrier, atrial natriuretic factor, horseradish peroxidase, lanthanum, ultrastructure.

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6

Glezer, Ilya I., Myron S. Jacobs, and Peter J. Morgane. "Ultrastructure of the blood-brain barrier in the dolphin (Stenella coeruleoalba)." Brain Research 414, no. 2 (June 1987): 205–18. http://dx.doi.org/10.1016/0006-8993(87)90001-1.

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7

Lamberts, R., and P. C. Goldsmith. "Fixation, fine structure, and immunostaining for neuropeptides: perfusion versus immersion of the neuroendocrine hypothalamus." Journal of Histochemistry & Cytochemistry 34, no. 3 (March 1986): 389–98. http://dx.doi.org/10.1177/34.3.2419392.

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The effects of various fixatives and fixation methods on ultrastructural morphology and the immunocytochemical localization of beta-endorphin were examined in rat brain. The mediobasal hypothalamus was preserved by vascular perfusion and/or immersion in nine different fixatives. We tested several combinations of paraformaldehyde, glutaraldehyde, acrolein, and picric acid in various isosmolar buffers. Vibratome sections were stained for beta-endorphin employing the peroxidase-antiperoxidase technique, or processed directly for electron microscopy. The ultrastructural quality of a given region was attributed to its location with respect to the blood-brain barrier, the method of fixation, and the concentrations of some of the fixative components. Immersion fixation gave better results and reduced extracellular space in the median eminence (outside the blood-brain barrier) and areas close to the hypothalamic surface. Positive immunostaining of beta-endorphin perikarya occurred only in tissue fixed with periodate-lysine-paraformaldehyde. Light to moderate fiber staining was also present in some paraformaldehyde-glutaraldehyde-acrolein combinations. However, a glutaraldehyde concentration of 1% or higher abolished all positive staining for beta-endorphin. These results emphasize the necessity of optimizing fixation for ultrastructure and for immunocytochemical staining of each individual antigen. The choice of the best fixation method depends not only on the intracellular location of the antigen but also on the relationship between hypothalamic tissue compartments and the blood-brain barrier.

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Stewart, P. A., M. Magliocco, K. Hayakawa, C. L. Farrell, R. F. Del Maestro, J. Girvin, J. C. E. Kaufmann, H. V. Vinters, and J. Gilbert. "A quantitative analysis of blood-brain barrier ultrastructure in the aging human." Microvascular Research 33, no. 2 (March 1987): 270–82. http://dx.doi.org/10.1016/0026-2862(87)90022-7.

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9

Greenwood, J., J. Adu, A. J. Davey, N. J. Abbott, and M. W. B. Bradbury. "The Effect of Bile Salts on the Permeability and Ultrastructure of the Perfused, Energy-Depleted, Rat Blood-Brain Barrier." Journal of Cerebral Blood Flow & Metabolism 11, no. 4 (July 1991): 644–54. http://dx.doi.org/10.1038/jcbfm.1991.116.

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The action of bile salts upon the rat blood–brain barrier (BBB) was assessed in the absence of energy-yielding metabolism. Brains were perfused in situ with a Ringer solution for 5 min followed by a 1 min perfusion containing either sodium deoxycholate (DOC), taurochenodeoxycholate (TCDC), or Ringer/DNP. The integrity of the BBB was then determined by perfusing with the radiotracer [14C]mannitol for 2.5 min. Alternatively, the brains were perfusion fixed for ultrastructural assessment. At 0.2 m M DOC, the BBB remained intact and the cerebral ultrastructure was similar to the controls. At 1 m M and above, disruption of the BBB became evident. At 2 m M, the cerebral cortex became severely vacuolated, with damaged endothelium and collapsed capillaries. With TCDC, BBB disruption occurred at 0.2 m M without any apparent ultrastructural damage to the micro vasculature. Following 2 m M TCDC, similar, but less widespread, structural changes to the 2 m M DOC-perfused animals was apparent. Opening of the BBB occurred at a concentration lower than that required to cause lysis of either red blood cells or cultured cerebral endothelial cells. It is proposed that the effect of bile salts at concentrations of 1.5 m M and above is largely due to their lytic action as strong detergents on endothelial cell membranes, but that at lower concentrations a more subtle modification of the BBB occurs.

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10

Nahirney, Patrick C., Patrick Reeson, and Craig E. Brown. "Ultrastructural analysis of blood–brain barrier breakdown in the peri-infarct zone in young adult and aged mice." Journal of Cerebral Blood Flow & Metabolism 36, no. 2 (October 2, 2015): 413–25. http://dx.doi.org/10.1177/0271678x15608396.

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Following ischemia, the blood–brain barrier is compromised in the peri-infarct zone leading to secondary injury and dysfunction that can limit recovery. Currently, it is uncertain what structural changes could account for blood–brain barrier permeability, particularly with aging. Here we examined the ultrastructure of early and delayed changes (3 versus 72 h) to the blood–brain barrier in young adult and aged mice (3–4 versus 18 months) subjected to photothrombotic stroke. At both time points and ages, permeability was associated with a striking increase in endothelial caveolae and vacuoles. Tight junctions were generally intact although small spaces were detected in a few cases. In young mice, ischemia led to a significant increase in pericyte process area and vessel coverage whereas these changes were attenuated with aging. Stroke led to an expansion of the basement membrane region that peaked at 3 h and partially recovered by 72 h in both age groups. Astrocyte endfeet and their mitochondria were severely swollen at both times points and ages. Our results suggest that blood–brain barrier permeability in young and aged animals is mediated by transcellular pathways (caveolae/vacuoles), rather than tight junction loss. Further, our data indicate that the effects of ischemia on pericytes and basement membrane are affected by aging.

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Dissertations / Theses on the topic "Blood-brain barrier Ultrastructure"

1

Sedlakova, Renata. "Ultrastructure of the blood-brain barrier in the rabbit." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq21077.pdf.

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Zhu, Chunni. "The Blood-brain barrier in normal and pathological conditions." Title page, abstract and contents only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phz637.pdf.

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Bibliography: leaves 318-367. Examines the blood-brain barrier in normal and pathological conditions induced by intravascular and extravascular insults. Intravascular insults were induced by administration of Clostridium perfringens prototoxin; extravascular insults were induced by an impact acceleration model for closed head injury to induce traumatic brain injury. Also examines the integrity of the blood-brain barrier ultrastructurally and by its ability to exclude endogenous and exogenous tracers. Also studies the expression of 2 blood-brain barrier specific proteins, endothelial barrier antigen (EBA) and glucose transporter 1 (GLUT1)

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Douglas, Andrew Graham Lim. "Oligonucleotide-based therapies for neuromuscular disease." Thesis, University of Oxford, 2015. http://ora.ox.ac.uk/objects/uuid:d14706a3-c436-46ff-87c4-40bbbad6dc01.

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Dyrna, Felix. "Systematic ultrastructural analyses of meningeal and parenchymal vessels of the central nervous system." 2018. https://ul.qucosa.de/id/qucosa%3A33633.

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The direct endothelial contact with adjacent astrocytic end-feet is believed to establish blood-brain barrier (BBB) typical characteristics in endothelial cells of the central nervous system (CNS). However, this contact is only present in capillary vessels of the brain parenchyma and absent in larger veins, arteries and vessels within the meninges. To investigate a potential impact of direct endothelial interactions with adjacent astrocytic end-feet on the molecular tight junction (TJ) composition and ultrastructure, we performed a systematic analysis of endothelial cell contacts within the vascular tree of parenchymal and leptomeningeal vessels. Immunofluorescence labeling for claudin-3, claudin-5, zonula occludens-1 and occludin was used to compare the molecular composition, without showing significant differences in their distribution along the vascular tree of parenchymal and leptomeningeal vessels. Furthermore, electron microscopy in combination with quantitative analyses was performed to investigate the endothelial ultrastructure revealing significant differences within the length of endothelial overlaps between the different vessel types. Here, parenchymal arteries exhibit noticeably longer cell contacts compared to capillaries, which could not be observed in leptomeningeal vessels. It was also observed that arterial vessels regularly contain a higher density of endothelial vesicles throughout the parenchyma and meninges as a sign for transendothelial traffic. Hence, endothelial expression of blood-brain barrier typical TJs is not limited to capillary vessels with an intimate contact to surrounding astrocytes, but is also observed in arteries and veins of the brain parenchyma as well as the meninges, the latter of which are lacking a direct astrocyte-endothelial interaction. These vessel-specific characteristics can now be used to address and compare alterations of the BBB in different settings of CNS pathologies.:Table of Content 1. INTRODUCTION 4 1.1 THE BLOOD-BRAIN BARRIER 4 1.2 HISTORY 5 1.3 STRUCTURE AND COMPOSITION 6 1.4 THE ROLE OF THE MICROENVIRONMENT 8 1.4.1 ASTROCYTES 8 1.4.2 PERICYTES 9 1.5 BLOOD BRAIN BARRIER FUNCTION 10 1.5.1 PHYSIOLOGIC CONDITIONS 10 1. 5.2 PATHOLOGIC CONDITIONS 11 2. OPEN QUESTIONS AND SCIENTIFIC APPROACH 12 3. PUBLICATIONS 13 3.1 DIFFERENT SEGMENTS OF THE CEREBRAL VASCULATURE REVEAL SPECIFIC ENDOTHELIAL SPECIFICATIONS, WHILE TIGHT JUNCTION PROTEINS APPEAR EQUALLY DISTRIBUTED 13 3.2 THE BLOOD-BRAIN BARRIER 28 4. SUMMARY 40 5. REFERENCES 43 6. PROOF OF SIGNIFICANT CONTRIBUTION 48 7. DECLARATION OF ACADEMIC HONESTY 49 8. ACKNOWLEDGMENT 50 9. CURRICULUM VITAE 51

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Books on the topic "Blood-brain barrier Ultrastructure"

1

Ultrastructural cytochemistry of blood-brain barrier endothelia. Stuttgart: G. Fischer, 1988.

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2

Coomber, Brenda Lynn. Quantitative ultrastructure of endothelial cells from blood-brain barrier and permeable microvessels. 1986.

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Book chapters on the topic "Blood-brain barrier Ultrastructure"

1

Pavelka, Margit, and Jürgen Roth. "Blood-Brain Barrier, Synapses." In Functional Ultrastructure, 318–19. Vienna: Springer Vienna, 2010. http://dx.doi.org/10.1007/978-3-211-99390-3_163.

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Brightman, M. W. "Ultrastructure of Brain Endothelium." In Physiology and Pharmacology of the Blood-Brain Barrier, 1–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76894-1_1.

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