Статті в журналах: "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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5

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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8

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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Stewart, P. A., K. Hayakawa, E. Hayakawa, C. L. Farrell, and R. F. Del Maestro. "A quantitative study of blood-brain barrier permeability ultrastructure in a new rat glioma model." Acta Neuropathologica 67, no. 1-2 (March 1985): 96–102. http://dx.doi.org/10.1007/bf00688129.

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12

Stewart, Patricia A., Kay Hayakawa, Catherine L. Farrell, and Rolando F. Del Maestro. "Quantitative study of microvessel ultrastructure in human peritumoral brain tissue." Journal of Neurosurgery 67, no. 5 (November 1987): 697–705. http://dx.doi.org/10.3171/jns.1987.67.5.0697.

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✓ The form and function of blood vessels are determined by the cells that constitute their microenvironment. Brain tissue around tumors contains varying numbers of tumor cells that could influence local capillaries to lose their blood-brain barrier (BBB), as they do in the tumor itself. Microvascular permeability cannot be measured directly in humans but can be inferred from a knowledge of vessel ultrastructure. The authors have examined the vascular ultrastructure associated with the BBB in human peritumoral brain tissue for evidence of BBB compromise and to correlate BBB features with the cellular components of the vessel microenvironment. Light microscopic examination of brain tissue samples in patients with primary brain tumors showed that the tissue lying beyond the visible edge of the tumor ranged from essentially normal to grossly infiltrated with tumor cells. Although some of the vessels were structurally normal, the microvessels as a group had elongated junctional clefts (unfused regions) and an increase in the density of endothelial vesicles. Furthermore, the cleft index (the percentage of the junctional profile that is unfused) varied directly with the local cell density. A subpopulation of vessels enveloped by a layer of tumor cells was grossly abnormal. However, vessels that were not immediately invested by tumor cells also showed some abnormalities. It is concluded that tumor cells infiltrating peritumoral brain tissue cause blood vessels to take on some of the structural characteristics of leaky vessels. Since direct contact is not required, and since the degree of abnormality correlates with the number of tumor cells in the environment, the authors suggest that this inductive influence is exerted over a distance and is dependent on the concentration of the inducing factors.

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13

Hong, Fashui, Xu Mu, Yuguan Ze, Wuyan Li, Yingjun Zhou, and Jianhui Ji. "Damage to the Blood Brain Barrier Structure and Function from Nano Titanium Dioxide Exposure Involves the Destruction of Key Tight Junction Proteins in the Mouse Brain." Journal of Biomedical Nanotechnology 17, no. 6 (June 1, 2021): 1068–78. http://dx.doi.org/10.1166/jbn.2021.3083.

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Numerous studies have proven that nano titanium dioxide (nano TiO2) can accumulate in animal brains, where it damages the blood brain barrier (BBB); however, whether this process involves destruction of tight junction proteins in the mouse brain has not been adequately investigated. In this study, mice were exposed to nano TiO2 for 30 consecutive days, and then we used transmission electron microscopy to observe the BBB ultrastructure and the Evans blue assay to evaluate the permeability of the BBB. Our data suggested that nano TiO2 damaged the BBB ultrastructure and increased BBB permeability. Furthermore, we used immunofluorescence and Western blotting to examine the expression of key tight junction proteins, including Occludin, ZO-1, and Claudin-5 in the mouse brain. Our data showed that nano TiO2 reduced Occludin, ZO-1 and Claudin-5 expression. Taken together, nano TiO2-induced damage to the BBB structure and function may involve the destruction of key tight junction proteins.

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14

Satomoto, Maiko, Zhongliang Sun, Yushi U. Adachi, and Koshi Makita. "Sugammadex-Enhanced Neuronal Apoptosis following Neonatal Sevoflurane Exposure in Mice." Anesthesiology Research and Practice 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/9682703.

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In rodents, neonatal sevoflurane exposure induces neonatal apoptosis in the brain and results in learning deficits. Sugammadex is a new selective neuromuscular blockade (NMB) binding agent that anesthesiologists can use to achieve immediate reversal of an NMB with few side effects. Given its molecular weight of 2178, sugammadex is thought to be unable to pass through the blood brain barrier (BBB). Volatile anesthetics can influence BBB opening and integrity. Therefore, we investigated whether the intraperitoneal administration of sugammadex could exacerbate neuronal damage following neonatal 2% sevoflurane exposure via changes in BBB integrity. Cleaved caspase-3 immunoblotting was used to detect apoptosis, and the ultrastructure of the BBB was examined by transmission electron microscopy. Exposure to 2% sevoflurane for 6 h resulted in BBB ultrastructural abnormalities in the hippocampus of neonatal mice. Sugammadex alone without sevoflurane did not induce apoptosis. The coadministration of sugammadex with sevoflurane to neonatal mice caused a significant increase (150%) in neuroapoptosis in the brain compared with 2% sevoflurane. In neonatal anesthesia, sugammadex could influence neurotoxicity together with sevoflurane. Exposure to 2% sevoflurane for 6 h resulted in BBB ultrastructural abnormalities in the hippocampus of neonatal mice.

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15

Tu, Jian, Marcus A. Stoodley, Michael K. Morgan, and Kingsley P. Storer. "Ultrastructural characteristics of hemorrhagic, nonhemorrhagic, and recurrent cavernous malformations." Journal of Neurosurgery 103, no. 5 (November 2005): 903–9. http://dx.doi.org/10.3171/jns.2005.103.5.0903.

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Object. Ultrastructural characteristics of hemorrhagic, nonhemorrhagic, primary, and recurrent central nervous system cavernous malformations (CMs) were examined in an attempt to clarify their pathological mechanisms. Methods. Thirteen specimens (nine from samples of CMs and four from healthy control tissue) were processed for ultrastructural study immediately after surgical or postmortem removal, by fixation in glutaraldehyde/formalin and postfixation in OsO4. Transmission electron microscopy was used to examine the vascular walls, endothelium, subendothelium, and cytoplasmic organelles. The vascular walls in CMs demonstrated abnormal ultrastructure with no basement membranes and astrocytic foot processes. Pericytes were rarely seen. Single-layer lining endothelial cells showed fenestrated luminal surfaces. Large gaps were observed at intercellular junctions between endothelial cells, and large vesicles with extremely thin plasma membranes bordering the lumen were common in the lesions that had previously hemorrhaged. Endothelial cells of recurrent CMs had more Weibel—Palade bodies, filopodia, cytoplasmic processes, micropinocytotic vesicles, and filaments than those in primary lesions and normal control tissues. Conclusions. The absence of the blood–brain barrier, normal supporting wall structure, and large vesicles bordering the lumen of CM vessels may explain leakage of red blood cells into surrounding brain in the absence of major hemorrhage. Proliferation of residual abnormal endothelial cells may contribute to the recurrence of surgically removed CMs.

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Lan, Rui, Jun Xiang, Guo-Hua Wang, Wen-Wei Li, Wen Zhang, Li-Li Xu, and Ding-Fang Cai. "Xiao-Xu-MingDecoction Protects against Blood-Brain Barrier Disruption and Neurological Injury Induced by Cerebral Ischemia and Reperfusion in Rats." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/629782.

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Xiao-Xu-Mingdecoction (XXMD) is an effective prescription in the treatment of ischemic stroke, but the mechanisms involved are not well known. In the present study, 120 male Sprague-Dawley rats were randomly divided into 5 groups: sham control (sham), ischemia and reperfusion (IR), and IR plus 15, 30, and 60 g/kg/day XXMD. The stroke model was induced by 90 min of middle cerebral artery occlusion followed by reperfusion. The brain lesion areas were evaluated by 2,3,5-triphenyltetrazolium chloride staining, and neurological deficits were observed at different time points after reperfusion. Blood-brain barrier (BBB) disruption was evaluated by assessing brain water content and Evans blue content. Pathological changes in BBB ultrastructure were observed with transmission electron microscopy. MMP-9, -2, and VEGF expression levels were quantitatively determined by western blotting and immunohistochemistry. We found that XXMD (60 g/kg/day) treatment reduced cerebral infarct area, improved behavioral function, and attenuated ultrastructure damage and permeability of BBB following ischemia and reperfusion. Moreover, XXMD downregulated the expression levels of MMP-9, -2, and VEGF. These findings indicate that XXMD alleviates BBB disruption and cerebral ischemic injury, which may be achieved by inhibiting the expression of MMP-9, -2, and VEGF.

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Sekaran, Hema, Chee-Yuen Gan, Aishah A. Latiff, Thomas Michael Harvey, Liyana Mohd Nazri, Nur Aziah Hanapi, Juzaili Azizi, and Siti R. Yusof. "Changes in blood-brain barrier permeability and ultrastructure, and protein expression in a rat model of cerebral hypoperfusion." Brain Research Bulletin 152 (October 2019): 63–73. http://dx.doi.org/10.1016/j.brainresbull.2019.07.010.

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Herde, Michel K., Katrin Geist, Rebecca E. Campbell, and Allan E. Herbison. "Gonadotropin-Releasing Hormone Neurons Extend Complex Highly Branched Dendritic Trees Outside the Blood-Brain Barrier." Endocrinology 152, no. 10 (July 26, 2011): 3832–41. http://dx.doi.org/10.1210/en.2011-1228.

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GnRH neurons project axons to the median eminence to control pituitary release of gonadotropins and, as such, represent the principal output neurons of the neuronal network controlling fertility. It is well established that the GnRH neurons exhibit a simple bipolar morphology with one or two long dendrites. Using adult GnRH-green fluorescent protein transgenic mice and juxtacellular cell filling, we report here that a subpopulation of GnRH neurons located in the rostral preoptic area exhibit extremely complex branching dendritic trees that fill the organum vasculosum of the lamina terminalis (OVLT). The dendritic nature of these processes was demonstrated at both light and electron microscopic levels by the presence of spines, dendritic ultrastructure, and synapses. Further, electrophysiological recordings showed that GnRH neurons were excited by glutamate as well as kisspeptin puffed onto their dendrites located within the OVLT. Using iv injection of horseradish peroxidase, a molecule unable to penetrate the blood-brain barrier (BBB), we show that GnRH neuron cell bodies and dendrites within 100 μm of the OVLT reside outside the BBB. Approximately 85% of GnRH neurons in this area express c-Fos at the time of the GnRH surge. These observations demonstrate that GnRH neurons extend complex, highly branched dendritic trees beyond the BBB into the OVLT, where they will be able to sense directly molecules circulating in the bloodstream. This indicates a new mechanism for the modulation of GnRH neurons that extends considerably the range of factors that are integrated by these neurons for the control of fertility.

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19

Traber, Peter G., Mauro Dal Canto, Daniel R. Ganger, and Andres T. Blei. "Electron microscopic evaluation of brain edema in rabbits with galactosamine-induced fulminant hepatic failure: Ultrastructure and integrity of the blood-brain barrier." Hepatology 7, no. 6 (November 1987): 1272–77. http://dx.doi.org/10.1002/hep.1840070616.

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20

Winkler, Lars, Rosel Blasig, Olga Breitkreuz-Korff, Philipp Berndt, Sophie Dithmer, Hans C. Helms, Dmytro Puchkov, et al. "Tight junctions in the blood–brain barrier promote edema formation and infarct size in stroke – Ambivalent effects of sealing proteins." Journal of Cerebral Blood Flow & Metabolism 41, no. 1 (February 13, 2020): 132–45. http://dx.doi.org/10.1177/0271678x20904687.

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The outcome of stroke is greatly influenced by the state of the blood–brain barrier (BBB). The BBB endothelium is sealed paracellularly by tight junction (TJ) proteins, i.e., claudins (Cldns) and the redox regulator occludin. Functions of Cldn3 and occludin at the BBB are largely unknown, particularly after stroke. We address the effects of Cldn3 deficiency and stress factors on the BBB and its TJs. Cldn3 tightened the BBB for small molecules and ions, limited endothelial endocytosis, strengthened the TJ structure and controlled Cldn1 expression. After middle cerebral artery occlusion (MCAO) and 3-h reperfusion or hypoxia of isolated brain capillaries, Cldn1, Cldn3 and occludin were downregulated. In Cldn3 knockout mice (C3KO), the reduction in Cldn1 was even greater and TJ ultrastructure was impaired; 48 h after MCAO of wt mice, infarct volumes were enlarged and edema developed, but endothelial TJs were preserved. In contrast, junctional localization of Cldn5 and occludin, TJ density, swelling and infarction size were reduced in affected brain areas of C3KO. Taken together, Cldn3 and occludin protect TJs in stroke, and this keeps the BBB intact. However, functional Cldn3, Cldn3-regulated TJ proteins and occludin promote edema and infarction, which suggests that TJ modulation could improve the outcome of stroke.

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Cao, Yiyun, Cheng Ni, Zhengqian Li, Lunxu Li, Yajie Liu, Chunyi Wang, Yanfeng Zhong, Dehua Cui, and Xiangyang Guo. "Isoflurane anesthesia results in reversible ultrastructure and occludin tight junction protein expression changes in hippocampal blood–brain barrier in aged rats." Neuroscience Letters 587 (February 2015): 51–56. http://dx.doi.org/10.1016/j.neulet.2014.12.018.

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Dong, Qian, Lin He, Linbo Chen, and Qiongzhen Deng. "Opening the Blood-Brain Barrier and Improving the Efficacy of Temozolomide Treatments of Glioblastoma Using Pulsed, Focused Ultrasound with a Microbubble Contrast Agent." BioMed Research International 2018 (November 11, 2018): 1–9. http://dx.doi.org/10.1155/2018/6501508.

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Objective.To explore the effects of pulsed, focused, and microbubble contrast agent-enhanced ultrasonography (mCEUS) on blood-brain barrier (BBB) permeability and the efficacy temozolomide for glioblastoma.Methods.Wistar rats (n = 30) were divided into three groups (n = 10 per group) to determine optimal CUES conditions for achieving BBB permeability, as assessed by ultrastructure transmission electron microscopy (TEM) and western blot assays for the tight junction protein claudin-5. Optimized mCEUS effects on BBB permeability were subsequently confirmed with Evans blue staining (2 groups of 10 rats). The glioma cell line 9L was injected into the brain striatum of Wistar rats. After temozolomide chemotherapy, we detected glial fibrillary acidic protein (GFAP) levels in serum by enzyme-linked immunosorbent assay (ELISA) and in brain tissue by western blot, immunocytochemistry, and real-time quantitative polymerase chain reaction (qPCR).Results.BBB permeability was maximized with 1 ml/kg contrast agent mCEUS delivered via 10-min intermittent launches with a 400-ms interval. Evans blue staining confirmed BBB permeability following ultrasonic cavitation in the control group (P < 0.05). Following temozolomide chemotherapy, levels of the tumor marker GFAP were increased in the group with ultrasonic cavitation compared with the control group (P < 0.05).Conclusions.When rats were treated by mCEUS with intermittent launches (interval, 400 ms) and injected with 1 mg/kg contrast agent, BBB permeability was increased and temozolomide BBB penetration was enhanced, therapeutic enhancement for glioblastoma.

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Lukaszevicz, Anne-Claire, Nathalie Sampaïo, Christelle Guégan, Alexandra Benchoua, Cécile Couriaud, Elisabeth Chevalier, Brigitte Sola, Pierre Lacombe, and Brigitte Onténiente. "High Sensitivity of Protoplasmic Cortical Astroglia to Focal Ischemia." Journal of Cerebral Blood Flow & Metabolism 22, no. 3 (March 2002): 289–98. http://dx.doi.org/10.1097/00004647-200203000-00006.

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The generally accepted concept that astrocytes are highly resistant to hypoxic/ischemic conditions has been challenged by an increasing amount of data. Considering the differences in functional implications of protoplasmic versus fibrous astrocytes, the authors have investigated the possibility that those discrepancies come from specific behaviors of the two cell types. The reactivity and fate of protoplasmic and fibrous astrocytes were observed after permanent occlusion of the medial cerebral artery in mice. A specific loss of glial fibrillary acidic protein (GFAP) immunolabeling in protoplasmic astrocytes occurred within minutes in the area with total depletion of regional CBF (rCBF) levels, whereas “classical” astrogliosis was observed in areas with remaining rCBF. Severe disturbance of cell function, as suggested by decreased GFAP content and increased permeability of the blood–brain barrier to macromolecules, was rapidly followed by necrotic cell death, as assessed by ultrastructure and by the lack of activation of the apoptotic protease caspase-3. In contrast to the response of protoplasmic astrocytes, fibrous astrocytes located at the brain surface and in deep cortical layers displayed a transient and limited hypertrophy, with no conspicuous cell death. These results point to a differential sensitivity of protoplasmic versus fibrous cortical astrocytes to blood deprivation, with a rapid demise of the former, adding to the suggestion that protoplasmic astrocytes play a crucial role in the pathogenesis of ischemic injury.

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Hirunagi, Kanjun, Elke Rommel, and Horst-W. Korf. "Ultrastructure of cerebrospinal fluid-contacting neurons immunoreactive to vasoactive intestinal peptide and properties of the blood-brain barrier in the lateral septal organ of the duck." Cell and Tissue Research 279, no. 1 (December 1, 1994): 123–33. http://dx.doi.org/10.1007/s004410050269.

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25

Hirunagi, Kanjun, Elke Rommel, and Horst-W. Korf. "Ultrastructure of cerebrospinal fluid-contacting neurons immunoreactive to vasoactive intestinal peptide and properties of the blood-brain barrier in the lateral septal organ of the duck." Cell & Tissue Research 279, no. 1 (January 1995): 123–33. http://dx.doi.org/10.1007/bf00300699.

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26

Zhào, Hóngyi, Yu Liu, Jing Zeng, Dandan Li, Weiwei Zhang, and Yonghua Huang. "Troxerutin and Cerebroprotein Hydrolysate Injection Protects Neurovascular Units from Oxygen-Glucose Deprivation and Reoxygenation-Induced Injury In Vitro." Evidence-Based Complementary and Alternative Medicine 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/9859672.

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Cerebral ischemia/reperfusion (I/R) injury involves complex events of cellular and molecular processes. Previous studies suggest that a neurovascular unit (NVU) acts as an intricate network to maintain the neuronal homeostatic microenvironment. The present study established an NVU model for oxygen-glucose deprivation and reoxygenation (OGD/R) damage, trying to target the major components of the NVU using a coculture of rat neurons, astrocytes, and rat brain microvascular endothelial cells (rBMECs) to investigate the therapeutic effects of troxerutin and cerebroprotein hydrolysate injections (TCHis). The study observed that OGD/R downregulated the expressions of GAP-43, Claudin-5, and AQP-4 obviously detected by Western blotting and immunocytochemical analysis, respectively, while TCHi ameliorated the effect of OGD/R significantly. Meanwhile, TCHi alleviated the abnormalities of ultrastructure of neurons and rBMECs induced by OGD/R. Furthermore, both levels of inflammatory cytokines (IL-1β, IL-6, and TNF-α) and cell adhesion molecules (VCAM-1 and ICAM-1) detected by ELISA in NVU supernatant were found elevated significantly through OGD/R, but TCHi ameliorated the trend. In addition, TCHi also mitigated the increase of proapoptotic factors (Bax, p53, and caspase-3) induced by OGD/R in NVU model statistically. All these findings demonstrated that TCHis played a protective role, which was reflected in anti-inflammation, antiapoptosis, and blood–brain barrier maintenance. The results of the study concluded that the NVU is an ideal target and TCHi acts as a neuroprotective agent against cerebral I/R injuries.

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Aliev, Gjumrakch, Joséph Charles Lamanna, Ludis Morales Álvarez, Mark Eric Obrenovich, Gerardo Jesús Pacheco, Hector Palacios, Eldar Qasimov, and Brianna Walrafen. "Oxidative stress-induced mitochondrial failure and vasoactive substances as key initiators of pathology favor the reclassification of Alzheimer Disease as a vasocognopathy." Nova 6, no. 10 (December 15, 2008): 170. http://dx.doi.org/10.22490/24629448.408.

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Alzheimer disease and cerebrovascular accident are two leading causes of age-related dementia. Increasing evidence supports the idea that chronic hypoperfusion is primarily responsible for the pathogenesis that underlies both disease processes. Hypoperfusion is associated with oxidative imbalance, largely due to reactive oxygen species, which is associated with other age-related degenerative disorders. Recent evidence indicates that a chronic injury stimulus induces the hypoperfusion seen in the microcirculation of vulnerable regions of the brain. This leads to energy failure, manifested by damaged mitochondrial ultrastructure. Mitochondrial derangements lead to the formation of a large number of electron-dense, ¿hypoxic¿ mitochondria and cause the overproduction of mitochondrial DNA (mtDNA) deletions, which is most likely due to double stranded breaks. Additionally, these mitochondrial abnormalities coexist with increased redox metal activity, lipid peroxidation, and RNA oxidation, all of which are well established features of Alzheimer disease pathology, prior to the appearance of amyloid b deposition. Alzheimer disease, oxidative stress occurs within various cellular compartments and within certain cell types more than others, namely the vascular endothelium, which is associated with atherosclerotic damage, as well as in pyramidal neurons and glia. Interestingly, these vulnerable cells show mtDNA deletions and oxidative stress markers only in the regions that are closely associated with damaged vessels. This evidence strongly suggests that chronic hypoperfusion induces the accumulation of the oxidative stress products. Furthermore, brain vascular wall lesions linearly correlate with the degree of neuronal and glial cell damage. We, therefore, conclude that chronic hypoperfusion is a key initiator of oxidative stress in various brain parenchymal cells, and the mitochondria appear to be primary targets for brain damage in Alzheimer disease. In this manuscript, we outline a role for the continuous accumulation of oxidative stress products, such as an abundance of nitric oxide products (via the overexpression of inducible and/or neuronal NO synthase (iNOS and nNOS respectively) and peroxynitrite accumulation, as secondary but accelerating factors compromising the blood brain barrier (BBB). If this turns out to be the case, pharmacological interventions that target chronic hypoperfusion might ameliorate the key features of dementing neurodegeneration.

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Vorbrodt, Andrzej W. "Ultrastructural Cytochemistry of Blood-Brain Barrier Endothelia." Progress in Histochemistry and Cytochemistry 18, no. 3 (January 1988): III—96. http://dx.doi.org/10.1016/s0079-6336(88)80001-9.

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29

Faso, L., R. S. Trowbridge, R. C. Moretz, and H. M. Wisniewski. "An ultrastructural study of isolated small vessel endothelial and choroid plexus epithelial cells of ovine brain." Proceedings, annual meeting, Electron Microscopy Society of America 49 (August 1991): 162–63. http://dx.doi.org/10.1017/s0424820100085113.

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Homeostasis in the central nervous system is maintained by two selective permeability barriers: the blood brain barrier (BBB), made up of capillary endothelial cells (ECs) and the blood cerebral spinal fluid barrier composed of specialized cuboidal epithelial (Ep) cells. The ECs of the BBB contain few profiles of trans-cellular pinocytotic vesicles and form a band of intercellular zonular occludens (ZO) sealing adjacent cells. Choroid plexus Ep cells have on their free surfaces microvilli that are irregularly oriented and expanded at the tips. They also contain juxtaluminal ZO which seal the intercellular spaces. Two cell types, small vessel endothelial cells (ECl) and choroid plexus epithelial cells (SCP), were isolated from ovine brain and established as cell strains. These cells were examined with scanning (SEM) and transmission electron microscopy (TEM) to determine if they retain the features characteristic of the cells in vivo.

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30

Stolp, H. B., P. A. Johansson, M. D. Habgood, K. M. Dziegielewska, N. R. Saunders, and C. J. Ek. "Effects of Neonatal Systemic Inflammation on Blood-Brain Barrier Permeability and Behaviour in Juvenile and Adult Rats." Cardiovascular Psychiatry and Neurology 2011 (March 10, 2011): 1–10. http://dx.doi.org/10.1155/2011/469046.

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Several neurological disorders have been linked to inflammatory insults suffered during development. We investigated the effects of neonatal systemic inflammation, induced by LPS injections, on blood-brain barrier permeability, endothelial tight junctions and behaviour of juvenile (P20) and adult rats. LPS-treatment resulted in altered cellular localisation of claudin-5 and changes in ultrastructural morphology of a few cerebral blood vessels. Barrier permeability to sucrose was significantly increased in LPS treated animals when adult but not at P20 or earlier. Behavioural tests showed that LPS treated animals at P20 exhibited altered behaviour using prepulse inhibition (PPI) analysis, whereas adults demonstrated altered behaviour in the dark/light test. These data indicate that an inflammatory insult during brain development can change blood-brain barrier permeability and behaviour in later life. It also suggests that the impact of inflammation can occur in several phases (short- and long-term) and that each phase might lead to different behavioural modifications.

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31

Qin, Delong, Junmin Wang, Anh Le, Tom J. Wang, Xuemei Chen, and Jian Wang. "Traumatic Brain Injury: Ultrastructural Features in Neuronal Ferroptosis, Glial Cell Activation and Polarization, and Blood–Brain Barrier Breakdown." Cells 10, no. 5 (April 24, 2021): 1009. http://dx.doi.org/10.3390/cells10051009.

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The secondary injury process after traumatic brain injury (TBI) results in motor dysfunction, cognitive and emotional impairment, and poor outcomes. These injury cascades include excitotoxic injury, mitochondrial dysfunction, oxidative stress, ion imbalance, inflammation, and increased vascular permeability. Electron microscopy is an irreplaceable tool to understand the complex pathogenesis of TBI as the secondary injury is usually accompanied by a series of pathologic changes at the ultra-micro level of the brain cells. These changes include the ultrastructural changes in different parts of the neurons (cell body, axon, and synapses), glial cells, and blood–brain barrier, etc. In view of the current difficulties in the treatment of TBI, identifying the changes in subcellular structures can help us better understand the complex pathologic cascade reactions after TBI and improve clinical diagnosis and treatment. The purpose of this review is to summarize and discuss the ultrastructural changes related to neurons (e.g., condensed mitochondrial membrane in ferroptosis), glial cells, and blood–brain barrier in the existing reports of TBI, to deepen the in-depth study of TBI pathomechanism, hoping to provide a future research direction of pathogenesis and treatment, with the ultimate aim of improving the prognosis of patients with TBI.

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32

Cornford, Eain M., Shigeyo Hyman, and Barbara E. Swartz. "The Human Brain GLUT1 Glucose Transporter: Ultrastructural Localization to the Blood—Brain Barrier Endothelia." Journal of Cerebral Blood Flow & Metabolism 14, no. 1 (January 1994): 106–12. http://dx.doi.org/10.1038/jcbfm.1994.15.

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Immunogold electron microscopy was used to examine human brain resections to localize the GLUT1 glucose transporter. The tissue examined was obtained from a patient undergoing surgery for treatment of seizures, and the capillary profiles examined had characteristics identical to those described previously for active, epileptogenic sites (confirmed by EEG analyses). A rabbit polyclonal antiserum to the full-length human erythrocyte glucose transporter (GLUT1) was labeled with 10-nm gold particle-secondary antibody conjugates and localized immunoreactive GLUT1 molecules in human brain capillary endothelia, with <0.25% of the particles beyond the capillary profile. Erythrocyte membranes were also highly immunoreactive, whereas macrophage membranes were GLUT1-negative. The number of immunoreactive sites per capillary profile was observed to be 10-fold greater in humans than in previous studies of rat and rabbit brain capillaries. In addition, half of the total number of immunoreactive gold particles were localized to the luminal capillary membrane. We suggest that the blood–brain barrier GLUT1 glucose transporter is up-regulated in seizures, and this elevated transporter activity is characterized by increased GLUT1 transporters, particularly on the luminal capillary membranes. In addition, acute modulation of glucose transporter activity is presumed to involve translocation of GLUT1 from cytoplasmic to luminal membrane sites, demonstrable with quantitative immunogold electron microscopy.

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Greenwood, J., A. S. Hazell, and P. J. Luthert. "The Effect of a Low pH Saline Perfusate upon the Integrity of the Energy-Depleted Rat Blood-Brain Barrier." Journal of Cerebral Blood Flow & Metabolism 9, no. 2 (April 1989): 234–42. http://dx.doi.org/10.1038/jcbfm.1989.34.

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The effect of a low pH perfusate upon the integrity of the rat blood-brain barrier was studied using an in situ supravital brain perfusion technique in which high-energy phosphates are depleted. Control animals were perfused for 10 min with a Ringer's salt solution containing the metabolic inhibitor 2,4-dinitrophenol (DNP) and adjusted to a pH of 7.4. In two separate experimental groups the perfusate, consisting of either the same medium as the controls or with additional buffering from Tris maleate, was switched after 5 min at a pH of 7.4, to a medium adjusted to pH 5.5 with lactic acid. Following a total perfusion time of 10 min, the integrity of the blood-brain barrier was assessed using the small molecular weight tracer [14C]mannitol. The cerebral perfusate flow rates (CPFR) after 10 min of perfusion were also determined in the three groups by perfusing for 40 s with [14C]iodoantipyrine. In each group, mannitol was excluded from the tissue of the brain to the same degree as has been previously reported in vivo, indicating an intact blood-brain barrier. There was also no significant pH-dependent change in CPFR. Ultrastructural examination of animals that had been perfusion fixed following in situ perfusion revealed no obvious differences between the cerebral endothelium of the control and low pH perfused animals. These results demonstrate that in the absence of energy-producing metabolism a perfusate pH of 5.5 is insufficient to disrupt the blood-brain barrier.

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34

Chen, Jinfeng, Zhixiong Lin, and Wei Wang. "CT-ultrastructural correlation study of the blood brain barrier in cerebral gliomas." Clinical Neurology and Neurosurgery 99 (July 1997): S85. http://dx.doi.org/10.1016/s0303-8467(97)81662-9.

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35

Stewart, P. A., and K. Hayakawa. "Early ultrastructural changes in blood-brain barrier vessels of the rat embryo." Developmental Brain Research 78, no. 1 (March 1994): 25–34. http://dx.doi.org/10.1016/0165-3806(94)90005-1.

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36

Farrell, Catherine L., and William M. Pardridge. "Ultrastructural localization of blood-brain barrier-specific antibodies using immunogold-silver enhancement techniques." Journal of Neuroscience Methods 37, no. 2 (April 1991): 103–10. http://dx.doi.org/10.1016/0165-0270(91)90120-o.

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37

Zumkeller, M., H. G. Höllerhage, E. Reale, and H. Dietz. "Ultrastructural changes in the blood-brain barrier after nimodipine treatment and induced hypertension." Experimental Neurology 113, no. 3 (September 1991): 315–21. http://dx.doi.org/10.1016/0014-4886(91)90021-4.

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38

Roberts, R. L., R. E. Fine, and A. Sandra. "Receptor-mediated endocytosis of transferrin at the blood-brain barrier." Journal of Cell Science 104, no. 2 (February 1, 1993): 521–32. http://dx.doi.org/10.1242/jcs.104.2.521.

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Rat brains were perfuse with a transferrin-peroxidase conjugate (Tf-HRP) to characterize morphologically the endocytic pathway of transferrin in blood-brain barrier endothelial cells. Electron microscopic evaluation of rat brains perfused with Tf-HRP at 4 degrees C and subsequently warmed to 37 degrees C for brief periods of time (2 minutes) showed sequestration of Tf-HRP in clathrin coated pits and vesicles on the luminal membrane of the brain endothelium. After 5 minutes of warming, diaminobenzidine (DAB) reaction product was present in vesicular structures 250–500 nm in diameter and in associated tubules morphologically identified as large or sorting endosomes. Recycling endosomes were also heavily labelled at this time point. Almost no DAB reaction product remained in the cerebral endothelial cells when the warming period was longer than 15 minutes. Other rat brains were perfused with Tf-HRP at 30 degrees C for 15 minutes prior to fixation and DAB cytochemistry. In these studies, brain endothelial cells contained large amounts of DAB reaction product, mostly localized in 50–100 nm vesicles and tubules, often in the Golgi region of the cells. Coated pits and vesicles and large endosomes were also heavily labelled. Transcytosis of Tf-HRP was not identified in either perfusion protocol. Ultrastructural, indirect immunocytochemical localization of transferrin receptors showed that the transferrin receptor is highly polarized at the blood-brain barrier and is localized only on the apical membrane, in contrast to other polarized epithelial cells, like hepatocytes, in which the receptor is present on the basolateral membrane. The evidence supports an iron transport model in which iron-loaded transferrin is taken up by receptor-mediated endocytosis at the luminal membrane of brain capillaries. The iron then dissociates from transferrin in endosomal compartments and is transcytosed by unknown mechanisms, while the transferrin is retroendocytosed.

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39

Olude, M. A., F. E. Olopade, O. A. Mustapha, S. T. Bello, A. O. Ihunwo, J. Plendl, and J. O. Olopade. "Ultrastructural Morphology of the Ependyma and Choroid Plexus in the African Giant Rat (Cricetomys gambianus)." Folia Veterinaria 65, no. 1 (March 1, 2021): 45–53. http://dx.doi.org/10.2478/fv-2021-0006.

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Abstract Ependymal cells line the interface between the ventricular surfaces and the brain parenchyma. These cells, in addition to the choroid plexus, form the blood-brain barrier (BBB) and the blood-cerebrospinal fluid barrier (BCSFB) and serve important functions in the protection and regulation of brain metabolism. The African giant rat (AGR) has been used as sentinels to detect potential neuropathology arising from ecotoxicological pollutions. This study examined the lateral ventricular lining by using histology, immunohistochemistry and electron microscopy. Marked variations were observed in some regions of the ventricles which showed multi-layering of ependymal cells that differed from the typical single layered ependymal cells at the apical surface, while subependymal structures revealed indistinctive neuropil and glia following histological examinations. The ependymal cells which form the epithelial lining of the ventricles were comprised of cuboidal or low columnar cells, with the plasmalemma of abutting cells forming intercellular bridge appearing links by: tight junctions (zonula occludens), intermediate junctions (zonula adherens), desmosomes (macula adherens) and infrequent gap junctions. The choroid plexus revealed cells of Kolmer with several cilia and microvilli. The possible functional components of the ependyma and choroid plexus morphology of the AGR are discussed and thus provide a baseline for further research on the AGR brain.

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40

Hayden, Melvin, DeAna Grant, Annayya Aroor, and Vincent DeMarco. "Ultrastructural Remodeling of the Neurovascular Unit in the Female Diabetic db/db Model–Part II: Microglia and Mitochondria." Neuroglia 1, no. 2 (October 7, 2018): 311–26. http://dx.doi.org/10.3390/neuroglia1020021.

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Obesity, insulin resistance, and type 2 diabetes mellitus are associated with diabetic cognopathy. This study tested the hypothesis that neurovascular unit(s) (NVU) within cerebral cortical gray matter regions may depict abnormal cellular remodeling. The monogenic (Leprdb) female diabetic db/db [BKS.CgDock7m +/+Leprdb/J] (DBC) mouse model was utilized for this ultrastructural study. Upon sacrifice (20 weeks), left-brain hemispheres of the DBC and age-matched nondiabetic control C57BL/KsJ (CKC) mice were immediately immersion-fixed. We observed an attenuation/loss of endothelial blood–brain barrier tight/adherens junctions and pericytes, thickened basement membranes, adherent red and white blood cells, neurovascular unit microbleeds and pathologic remodeling of protoplasmic astrocytes. In this second of a three-part series, we focus on the observational ultrastructural remodeling of microglia and mitochondria in relation to the NVU in leptin receptor deficient DBC models. This study identified novel ultrastructural core signature remodeling changes, which consisted of invasive activated microglia, microglial aberrant mitochondria with nuclear chromatin condensation and adhesion of white blood cells to an activated endothelium of the NVU. In conclusion, the results implicate activated microglia in NVU uncoupling and the resulting ischemic neuronal and synaptic damage, which may be related to impaired cognition and diabetic cognopathy.

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41

Bhatt, Alok, and Justin Brucker. "Early Clinical Experiences with Positron Emission Tomography–Magnetic Resonance Imaging in Epilepsy: Implications for Modeling the Neurovascular Unit." Journal of Pediatric Neurology 16, no. 02 (July 19, 2017): 125–38. http://dx.doi.org/10.1055/s-0037-1604218.

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AbstractCortical function in normal and pathologic neurologic states is largely influenced by the activity of the neurovascular unit. Hybrid technologies that combine positron emission tomography and magnetic resonance imaging (PET/MRI) offer a chance for simultaneous noninvasive evaluation of cortical glucose consumption, blood flow, and cerebrovascular reactivity. We present differing PET/MRI results for two pediatric patients undergoing evaluation for medically refractory seizures, interpreted in the context of neurovascular unit behavior, suggesting the presence of ultrastructural changes at the level of the blood brain barrier in various epilepsy disorders.

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42

Hayden, Melvin R., and William A. Banks. "Deficient Leptin Cellular Signaling Plays a Key Role in Brain Ultrastructural Remodeling in Obesity and Type 2 Diabetes Mellitus." International Journal of Molecular Sciences 22, no. 11 (May 21, 2021): 5427. http://dx.doi.org/10.3390/ijms22115427.

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The triad of obesity, metabolic syndrome (MetS), Type 2 diabetes mellitus (T2DM) and advancing age are currently global societal problems that are expected to grow over the coming decades. This triad is associated with multiple end-organ complications of diabetic vasculopathy (maco-microvessel disease), neuropathy, retinopathy, nephropathy, cardiomyopathy, cognopathy encephalopathy and/or late-onset Alzheimer’s disease. Further, obesity, MetS, T2DM and their complications are associated with economical and individual family burdens. This review with original data focuses on the white adipose tissue-derived adipokine/hormone leptin and how its deficient signaling is associated with brain remodeling in hyperphagic, obese, or hyperglycemic female mice. Specifically, the ultrastructural remodeling of the capillary neurovascular unit, brain endothelial cells (BECs) and their endothelial glycocalyx (ecGCx), the blood-brain barrier (BBB), the ventricular ependymal cells, choroid plexus, blood-cerebrospinal fluid barrier (BCSFB), and tanycytes are examined in female mice with impaired leptin signaling from either dysfunction of the leptin receptor (DIO and db/db models) or the novel leptin deficiency (BTBR ob/ob model).

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43

Balkanov, A. S., V. P. Chernikov, and A. V. Golanov. "The role of ultrastructural abnormalities of the blood-brain barrier in the development of brain glioblastoma radioresistance." Almanac of Clinical Medicine 46, no. 7 (December 17, 2018): 682–89. http://dx.doi.org/10.18786/2072-0505-2018-46-7-682-689.

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44

Ceafalan, Laura Cristina, Tudor Emanuel Fertig, Teodora Cristina Gheorghe, Mihail Eugen Hinescu, Bogdan Ovidiu Popescu, Jens Pahnke, and Mihaela Gherghiceanu. "Age-related ultrastructural changes of the basement membrane in the mouse blood-brain barrier." Journal of Cellular and Molecular Medicine 23, no. 2 (November 19, 2018): 819–27. http://dx.doi.org/10.1111/jcmm.13980.

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45

Molnár, Peter P., Brian P. O'Neill, Bernd W. Scheithauer, and Dennis R. Groothuis. "The blood-brain barrier in primary CNS lymphomas: Ultrastructural evidence of endothelial cell death." Neuro-Oncology 1, no. 2 (April 1, 1999): 89–100. http://dx.doi.org/10.1093/neuonc/1.2.89.

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46

Molnár, Peter P., Brian P. O'Neill, Bernd W. Scheithauer, and Dennis R. Groothuis. "The blood-brain barrier in primary CNS lymphomas: Ultrastructural evidence of endothelial cell death." Neuro-Oncology 1, no. 2 (April 1, 1999): 89–100. http://dx.doi.org/10.1215/s152285179800009x.

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47

Molnar, P. P. "The blood-brain barrier in primary CNS lymphomas: Ultrastructural evidence of endothelial cell death." Neuro-Oncology 1, no. 2 (April 1, 1999): 89–100. http://dx.doi.org/10.1215/15228517-1-2-89.

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48

Claudio, Luz. "Ultrastructural features of the blood-brain barrier in biopsy tissue from Alzheimer's disease patients." Acta Neuropathologica 91, no. 1 (December 1, 1995): 6–14. http://dx.doi.org/10.1007/s004010050386.

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49

Mander, Kimberley A., Francisco A. Uzal, Ruth Williams, and John W. Finnie. "Clostridium perfringens type D epsilon toxin produces a rapid and dose-dependent cytotoxic effect on cerebral microvascular endothelial cells in vitro." Journal of Veterinary Diagnostic Investigation 32, no. 2 (October 14, 2019): 277–81. http://dx.doi.org/10.1177/1040638719882745.

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Clostridium perfringens type D epsilon toxin (ETX) is responsible for a severe and frequently fatal neurologic disorder in ruminant livestock. Light microscopic, immunohistochemical, and ultrastructural studies have suggested that ETX injury to the cerebral microvasculature, with subsequent severe, generalized vasogenic edema and increased intracranial pressure, is critically important in producing neurologic dysfunction. However, the effect of ETX on brain capillary endothelial cells in vitro has not been examined previously, to our knowledge. We exposed a well-characterized human blood–brain barrier cell line to increasing concentrations of ETX, and demonstrated a direct and dose-dependent endotheliotoxic effect. Our findings are concordant with the primacy of vasculocentric brain lesions in the diagnosis of acute epsilon toxin enterotoxemia in ruminant livestock.

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50

Wu, Jin-Song, Xian-Cheng Chen, Hong Chen, and Yu-Quan Shi. "A study on blood–brain barrier ultrastructural changes induced by cerebral hypoperfusion of different stages." Neurological Research 28, no. 1 (January 2006): 50–58. http://dx.doi.org/10.1179/016164106x91870.

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