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Готові списки джерел за темами / Blood-brain barrier Physiology / Статті в журналах

Щоб переглянути інші типи публікацій з цієї теми, перейдіть за посиланням: Blood-brain barrier Physiology.

Статті в журналах з теми "Blood-brain barrier Physiology"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 3 лютого 2022

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1

Dunn, Jeff F., and Albert M. Isaacs. "The impact of hypoxia on blood-brain, blood-CSF, and CSF-brain barriers." Journal of Applied Physiology 131, no. 3 (September 1, 2021): 977–85. http://dx.doi.org/10.1152/japplphysiol.00108.2020.

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The blood-brain barrier (BBB), blood-cerebrospinal fluid (CSF) barrier (BCSFB), and CSF-brain barriers (CSFBB) are highly regulated barriers in the central nervous system comprising complex multicellular structures that separate nerves and glia from blood and CSF, respectively. Barrier damage has been implicated in the pathophysiology of diverse hypoxia-related neurological conditions, including stroke, multiple sclerosis, hydrocephalus, and high-altitude cerebral edema. Much is known about the damage to the BBB in response to hypoxia, but much less is known about the BCSFB and CSFBB. Yet, it is known that these other barriers are implicated in damage after hypoxia or inflammation. In the 1950s, it was shown that the rate of radionucleated human serum albumin passage from plasma to CSF was five times higher during hypoxic than normoxic conditions in dogs, due to BCSFB disruption. Severe hypoxia due to administration of the bacterial toxin lipopolysaccharide is associated with disruption of the CSFBB. This review discusses the anatomy of the BBB, BCSFB, and CSFBB and the impact of hypoxia and associated inflammation on the regulation of those barriers.

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2

Koziara, J. M., P. R. Lockman, D. D. Allen, and R. J. Mumper. "The Blood-Brain Barrier and Brain Drug Delivery." Journal of Nanoscience and Nanotechnology 6, no. 9 (September 1, 2006): 2712–35. http://dx.doi.org/10.1166/jnn.2006.441.

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The present report encompasses a thorough review of drug delivery to the brain with a particular focus on using drug carriers such as liposomes and nanoparticles. Challenges in brain drug delivery arise from the presence of one of the strictest barriers in vivo—the blood-brain barrier (BBB). This barrier exists at the level of endothelial cells of brain vasculature and its role is to maintain brain homeostasis. To better understand the principles of brain drug delivery, relevant knowledge of the blood-brain barrier anatomy and physiology is briefly reviewed. Several approaches to overcome the BBB have been reviewed including the use of carrier systems. In addition, strategies to enhance brain drug delivery by specific brain targeting are discussed.

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3

McCaffrey, Gwen, and Thomas P. Davis. "Physiology and Pathophysiology of the Blood-Brain Barrier." Journal of Investigative Medicine 60, no. 8 (December 1, 2012): 1131–40. http://dx.doi.org/10.2310/jim.0b013e318276de79.

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4

Serlin, Yonatan, Ilan Shelef, Boris Knyazer, and Alon Friedman. "Anatomy and physiology of the blood–brain barrier." Seminars in Cell & Developmental Biology 38 (February 2015): 2–6. http://dx.doi.org/10.1016/j.semcdb.2015.01.002.

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5

Robinson, P. J. "MEASUREMENT OF BLOOD-BRAIN BARRIER PERMEABILITY." Clinical and Experimental Pharmacology and Physiology 17, no. 12 (December 1990): 829–40. http://dx.doi.org/10.1111/j.1440-1681.1990.tb01286.x.

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6

Tietz, Silvia, and Britta Engelhardt. "Brain barriers: Crosstalk between complex tight junctions and adherens junctions." Journal of Cell Biology 209, no. 4 (May 25, 2015): 493–506. http://dx.doi.org/10.1083/jcb.201412147.

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Анотація:

Unique intercellular junctional complexes between the central nervous system (CNS) microvascular endothelial cells and the choroid plexus epithelial cells form the endothelial blood–brain barrier (BBB) and the epithelial blood–cerebrospinal fluid barrier (BCSFB), respectively. These barriers inhibit paracellular diffusion, thereby protecting the CNS from fluctuations in the blood. Studies of brain barrier integrity during development, normal physiology, and disease have focused on BBB and BCSFB tight junctions but not the corresponding endothelial and epithelial adherens junctions. The crosstalk between adherens junctions and tight junctions in maintaining barrier integrity is an understudied area that may represent a promising target for influencing brain barrier function.

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7

Grant, Gerald A., N. Joan Abbott, and Damir Janigro. "Understanding the Physiology of the Blood-Brain Barrier: In Vitro Models." Physiology 13, no. 6 (December 1998): 287–93. http://dx.doi.org/10.1152/physiologyonline.1998.13.6.287.

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Endothelial cells exposed to inductive central nervous system factors differentiate into a blood-brain barrier phenotype. The blood-brain barrier frequently obstructs the passage of chemotherapeutics into the brain. Tissue culture systems have been developed to reproduce key properties of the intact blood-brain barrier and to allow for testing of mechanisms of transendothelial drug permeation.

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8

Ermisch, A., P. Brust, R. Kretzschmar, and H. J. Ruhle. "Peptides and blood-brain barrier transport." Physiological Reviews 73, no. 3 (July 1, 1993): 489–527. http://dx.doi.org/10.1152/physrev.1993.73.3.489.

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9

Sweeney, Melanie D., Zhen Zhao, Axel Montagne, Amy R. Nelson, and Berislav V. Zlokovic. "Blood-Brain Barrier: From Physiology to Disease and Back." Physiological Reviews 99, no. 1 (January 1, 2019): 21–78. http://dx.doi.org/10.1152/physrev.00050.2017.

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The blood-brain barrier (BBB) prevents neurotoxic plasma components, blood cells, and pathogens from entering the brain. At the same time, the BBB regulates transport of molecules into and out of the central nervous system (CNS), which maintains tightly controlled chemical composition of the neuronal milieu that is required for proper neuronal functioning. In this review, we first examine molecular and cellular mechanisms underlying the establishment of the BBB. Then, we focus on BBB transport physiology, endothelial and pericyte transporters, and perivascular and paravascular transport. Next, we discuss rare human monogenic neurological disorders with the primary genetic defect in BBB-associated cells demonstrating the link between BBB breakdown and neurodegeneration. Then, we review the effects of genes underlying inheritance and/or increased susceptibility for Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease, and amyotrophic lateral sclerosis (ALS) on BBB in relation to other pathologies and neurological deficits. We next examine how BBB dysfunction relates to neurological deficits and other pathologies in the majority of sporadic AD, PD, and ALS cases, multiple sclerosis, other neurodegenerative disorders, and acute CNS disorders such as stroke, traumatic brain injury, spinal cord injury, and epilepsy. Lastly, we discuss BBB-based therapeutic opportunities. We conclude with lessons learned and future directions, with emphasis on technological advances to investigate the BBB functions in the living human brain, and at the molecular and cellular level, and address key unanswered questions.

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10

Gray, Sarah M., and Eugene J. Barrett. "Insulin transport into the brain." American Journal of Physiology-Cell Physiology 315, no. 2 (August 1, 2018): C125—C136. http://dx.doi.org/10.1152/ajpcell.00240.2017.

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Анотація:

While there is a growing consensus that insulin has diverse and important regulatory actions on the brain, seemingly important aspects of brain insulin physiology are poorly understood. Examples include: what is the insulin concentration within brain interstitial fluid under normal physiologic conditions; whether insulin is made in the brain and acts locally; does insulin from the circulation cross the blood-brain barrier or the blood-CSF barrier in a fashion that facilitates its signaling in brain; is insulin degraded within the brain; do privileged areas with a “leaky” blood-brain barrier serve as signaling nodes for transmitting peripheral insulin signaling; does insulin action in the brain include regulation of amyloid peptides; whether insulin resistance is a cause or consequence of processes involved in cognitive decline. Heretofore, nearly all of the studies examining brain insulin physiology have employed techniques and methodologies that do not appreciate the complex fluid compartmentation and flow throughout the brain. This review attempts to provide a status report on historical and recent work that begins to address some of these issues. It is undertaken in an effort to suggest a framework for studies going forward. Such studies are inevitably influenced by recent physiologic and genetic studies of insulin accessing and acting in brain, discoveries relating to brain fluid dynamics and the interplay of cerebrospinal fluid, brain interstitial fluid, and brain lymphatics, and advances in clinical neuroimaging that underscore the dynamic role of neurovascular coupling.

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11

MAYHAN, WILLIAM G. "Regulation of Blood-Brain Barrier Permeability." Microcirculation 8, no. 2 (April 2001): 89–104. http://dx.doi.org/10.1111/j.1549-8719.2001.tb00160.x.

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12

Chabrier, P. E., P. Roubert, P. Plas, and P. Braquet. "Blood–brain barrier and atrial natriuretic factor." Canadian Journal of Physiology and Pharmacology 66, no. 3 (March 1, 1988): 276–79. http://dx.doi.org/10.1139/y88-047.

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Анотація:

In brain, binding sites for atrial natriuretic factor (ANF) have been characterized in areas such as circumventricular organs that lack the tight capillary endothelial junctions of the blood–brain barrier and therefore are exposed to circulating peptides. Since atrial natriuretic factor acts directly on vascular endothelium and has been proposed to be actively involved in blood pressure regulation and fluid homeostasis, it is interesting to know whether ANF receptors exist on brain capillaries that constitute the blood–brain barrier and participate in the constant fluid exchange between blood and brain. The present paper reports recent evidence of the presence of ANF receptors located on the structure. It assesses the specific binding of 125I-labelled ANF on bovine brain microvessel preparations and its coupling with a guanylate cyclase system. The potential physiological role of ANF on brain microcirculation and blood–brain barrier functions is discussed.

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13

Patel, Bhuvic, Peter H. Yang, and Albert H. Kim. "The effect of thermal therapy on the blood-brain barrier and blood-tumor barrier." International Journal of Hyperthermia 37, no. 2 (July 16, 2020): 35–43. http://dx.doi.org/10.1080/02656736.2020.1783461.

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14

Schulze, Dr C. "Understanding the Blood-Brain-Barrier." Neuropathology and Applied Neurobiology 23, no. 2 (April 1997): 150–51. http://dx.doi.org/10.1111/j.1365-2990.1997.tb01197.x.

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15

Schulze, C. "Understanding the Blood-Brain-Barrier." Neuropathology and Applied Neurobiology 23, no. 3 (June 1997): 150–51. http://dx.doi.org/10.1046/j.1365-2990.1997.t01-1-90098900.x.

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16

Cosolo, W. C., P. Martinello, W. J. Louis, and N. Christophidis. "Blood-brain barrier disruption using mannitol: time course and electron microscopy studies." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 2 (February 1, 1989): R443—R447. http://dx.doi.org/10.1152/ajpregu.1989.256.2.r443.

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Анотація:

Blood-brain barrier disruption with a hyperosmolar agent, mannitol, has previously been demonstrated to increase intracerebral methotrexate levels in rats. To determine the optimum conditions for blood-brain barrier disruption without producing neurological sequelae, adult Sprague-Dawley rats were infused with mannitol via the internal carotid artery at rates varying from 0.25 to 0.5 ml.s-1.kg-1. Methotrexate and Evans blue were used as markers of blood-brain barrier disruption. The optimum rate of mannitol that produced blood-brain barrier disruption without neurological sequelae was 0.25 ml.s-1.kg-1 for 20 s. The duration of blood-brain barrier opening was maximal for approximately 5 min and then rapidly reversed. Methotrexate levels on the mannitol-infused side were four to five times that of the noninfused hemisphere. Light microscopy and electron microscopy did not demonstrate any consistent changes that could be attributed to blood-brain barrier disruption nor did it elucidate the mechanism. This model should prove useful in the investigation of the treatment of intracerebral tumors with blood-brain barrier disruption. This study shows that maximal intracerebral methotrexate levels were obtained when methotrexate was infused before or within 5 min of the mannitol infusion.

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17

Robinson, P. J., and S. I. Rapoport. "Size selectivity of blood-brain barrier permeability at various times after osmotic opening." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 253, no. 3 (September 1, 1987): R459—R466. http://dx.doi.org/10.1152/ajpregu.1987.253.3.r459.

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Recent experiments have shown that after osmotic opening the blood-brain barrier recloses more rapidly to larger than to smaller molecules. Quantitative theoretical analysis of blood-brain barrier permeability to different-sized molecules at different times after osmotic opening supports the concept of pore creation as a result of opening of tight junctions between endothelial cells. Experiments also suggest significant bulk water flow from capillaries into brain within 10 min after opening at an average rate of approximately 1.6 X 10(-4) cm3 X s-1 X g brain-1. A mathematical model of blood-brain barrier permeability based on the creation of pores, together with bulk fluid flow, is presented for both cylindrical pores and rectangular slits. Experimental data are compatible with pore radii of approximately 200 A or slit widths of approximately 220 A. Pore densities of approximately 1 pore per 200 microns 2 of membrane surface are calculated at 6 min after barrier opening, reducing slightly as the barrier recloses. Calculated bulk flow is reduced by an order of magnitude within 35 min of barrier opening and is a major factor in altered blood-brain barrier permeability. Size dependence of blood-brain barrier permeability following osmotic opening is shown to be incompatible with enhanced vesicular transport.

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18

Scherrmann, J. M. "Drug delivery to brain via the blood–brain barrier." Vascular Pharmacology 38, no. 6 (June 2002): 349–54. http://dx.doi.org/10.1016/s1537-1891(02)00202-1.

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19

Dziegielewska, Katarzyna. "The Blood-Brain Barrier: Biology and Research Protocols." Clinical and Experimental Pharmacology and Physiology 31, no. 3 (March 2004): 195. http://dx.doi.org/10.1111/j.1440-1681.2004.03971.x.

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20

Pardridge, William M. "S1-01-01: Blood-brain barrier from physiology to therapeutics." Alzheimer's & Dementia 11, no. 7S_Part_2 (July 2015): P114. http://dx.doi.org/10.1016/j.jalz.2015.07.002.

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21

Pandit, Rucha, Liyu Chen, and Jürgen Götz. "The blood-brain barrier: Physiology and strategies for drug delivery." Advanced Drug Delivery Reviews 165-166 (2020): 1–14. http://dx.doi.org/10.1016/j.addr.2019.11.009.

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22

Wolburg, Hartwig, and Andrea Lippoldt. "Tight junctions of the blood–brain barrier." Vascular Pharmacology 38, no. 6 (June 2002): 323–37. http://dx.doi.org/10.1016/s1537-1891(02)00200-8.

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23

Hawkins, Brian T., Richard D. Egleton, and Thomas P. Davis. "Modulation of cerebral microvascular permeability by endothelial nicotinic acetylcholine receptors." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 1 (July 2005): H212—H219. http://dx.doi.org/10.1152/ajpheart.01210.2004.

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Nicotine increases the permeability of the blood-brain barrier in vivo. This implies a possible role for nicotinic acetylcholine receptors in the regulation of cerebral microvascular permeability. Expression of nicotinic acetylcholine receptor subunits in cerebral microvessels was investigated with immunofluorescence microscopy. Positive immunoreactivity was found for receptor subunits α3, α5, α7, and β2, but not subunits α4, β3, or β4. Blood-brain barrier permeability was assessed via in situ brain perfusion with [14C]sucrose. Nicotine increased the rate of sucrose entry into the brain from 0.3 ± 0.1 to 1.1 ± 0.2 μl·g−1·min−1, as previously described. This nicotine-induced increase in blood-brain barrier permeability was significantly attenuated by both the blood-brain barrier-permeant nicotinic antagonist mecamylamine and the blood-brain barrier-impermeant nicotinic antagonist hexamethonium to 0.5 ± 0.2 and 0.3 ± 0.2 μl·g−1·min−1, respectively. These data suggest that nicotinic acetylcholine receptors expressed on the cerebral microvascular endothelium mediate nicotine-induced changes in blood-brain barrier permeability.

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24

Hendricks, Benjamin K., Aaron A. Cohen-Gadol, and James C. Miller. "Novel delivery methods bypassing the blood-brain and blood-tumor barriers." Neurosurgical Focus 38, no. 3 (March 2015): E10. http://dx.doi.org/10.3171/2015.1.focus14767.

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Glioblastoma (GBM) is the most common primary brain tumor and carries a grave prognosis. Despite years of research investigating potentially new therapies for GBM, the median survival rate of individuals with this disease has remained fairly stagnant. Delivery of drugs to the tumor site is hampered by various barriers posed by the GBM pathological process and by the complex physiology of the blood-brain and blood–cerebrospinal fluid barriers. These anatomical and physiological barriers serve as a natural protection for the brain and preserve brain homeostasis, but they also have significantly limited the reach of intraparenchymal treatments in patients with GBM. In this article, the authors review the functional capabilities of the physical and physiological barriers that impede chemotherapy for GBM, with a specific focus on the pathological alterations of the blood-brain barrier (BBB) in this disease. They also provide an overview of current and future methods for circumventing these barriers in therapeutic interventions. Although ongoing research has yielded some potential options for future GBM therapies, delivery of chemotherapy medications across the BBB remains elusive and has limited the efficacy of these medications.

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25

Ezan, Pascal, Pascal André, Salvatore Cisternino, Bruno Saubaméa, Anne-Cécile Boulay, Suzette Doutremer, Marie-Annick Thomas, Nicole Quenech'du, Christian Giaume, and Martine Cohen-Salmon. "Deletion of Astroglial Connexins Weakens the Blood–Brain Barrier." Journal of Cerebral Blood Flow & Metabolism 32, no. 8 (April 4, 2012): 1457–67. http://dx.doi.org/10.1038/jcbfm.2012.45.

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Astrocytes, the most prominent glial cell type in the brain, send specialized processes named endfeet, which enwrap blood vessels and express a large molecular repertoire dedicated to the physiology of the vascular system. One of the most striking properties of astrocyte endfeet is their enrichment in gap junction protein connexins 43 and 30 (Cx43 and Cx30) allowing for direct intercellular trafficking of ions and small signaling molecules through perivascular astroglial networks. The contribution of astroglial connexins to the physiology of the brain vascular system has never been addressed. Here, we show that Cx43 and Cx30 expression at the level of perivascular endfeet starts from postnatal days 2 and 12 and is fully mature at postnatal days 15 and 20, respectively, indicating that astroglial perivascular connectivity occurs and develops during postnatal blood–brain barrier (BBB) maturation. We demonstrate that mice lacking Cx30 and Cx43 in GFAP (glial fibrillary acidic protein)-positive cells display astrocyte endfeet edema and a partial loss of the astroglial water channel aquaporin-4 and β-dystroglycan, a transmembrane receptor anchoring astrocyte endfeet to the perivascular basal lamina. Furthermore, the absence of astroglial connexins weakens the BBB, which opens upon increased hydrostatic vascular pressure and shear stress. These results demonstrate that astroglial connexins are necessary to maintain BBB integrity.

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26

Seo, Suyeong, Hwieun Kim, Jong Hwan Sung, Nakwon Choi, Kangwon Lee, and Hong Nam Kim. "Microphysiological systems for recapitulating physiology and function of blood-brain barrier." Biomaterials 232 (February 2020): 119732. http://dx.doi.org/10.1016/j.biomaterials.2019.119732.

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27

Mayhan, W. G., F. M. Faraci, and D. D. Heistad. "Disruption of the blood-brain barrier in cerebrum and brain stem during acute hypertension." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 6 (December 1, 1986): H1171—H1175. http://dx.doi.org/10.1152/ajpheart.1986.251.6.h1171.

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The purpose of this study was to examine hemodynamic mechanisms of protection of the blood-brain barrier in the brain stem during acute hypertension. We used a new method to examine the microcirculation of the brain stem. Intravital fluorescent microscopy and fluorescein-labeled dextran were used to evaluate disruption of the blood-brain barrier during acute hypertension in rats. During control conditions, pressure (servo null) in arterioles (60 microns in diameter) was 50 +/- 2% (mean +/- SE) of systemic arterial pressure in the cerebrum and 67 +/- 1% of systemic arterial pressure in the brain stem (P less than 0.05 vs. cerebrum). In the cerebrum, pial venous pressure increased from 7 +/- 1 to 25 +/- 2 mmHg during acute hypertension, and there was marked disruption of the blood-brain barrier in venules (26 +/- 2 leaky sites). In contrast, in the brain stem, pial venous pressure increased from 4 +/- 1 to only 8 +/- 1 mmHg (P less than 0.05 vs. cerebrum), and there was minimal disruption of the blood-brain barrier in venules (1.5 +/- 0.6 leaky sites, P less than 0.05 vs. cerebrum). During acute hypertension, increases in blood flow (microspheres) were less in brain stem than in cerebrum. The findings suggest distribution of vascular resistance differs in the brain stem and cerebrum under control conditions, whereas large arteries account for a greater fraction of resistance in cerebrum; pial venous pressure increases less in brain stem than cerebrum during acute hypertension, so that the blood-brain barrier is protected.(ABSTRACT TRUNCATED AT 250 WORDS)

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28

Harik, S. I., R. A. Behmand, and J. C. LaManna. "Hypoxia increases glucose transport at blood-brain barrier in rats." Journal of Applied Physiology 77, no. 2 (August 1, 1994): 896–901. http://dx.doi.org/10.1152/jappl.1994.77.2.896.

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Анотація:

Prolonged hypoxia causes several adaptive changes in systemic physiology and tissue metabolism. We studied the effects of hypobaric hypoxia on glucose transport at the blood-brain barrier (BBB) in the rat. We found that hypoxia increased the density of brain microvessels seen on immunocytochemical stains using an antibody to the glucose transporting protein GLUT. In addition, we found that hypoxia increased the density of GLUT in isolated cerebral microvessels as determined by specific cytochalasin B binding. The higher GLUT density in isolated cerebral microvessels was evident after 1 wk of hypoxia and was associated with decreased activity of gamma-glutamyltranspeptidase. Consistent with these findings, we also demonstrated that 3 wk of hypobaric hypoxia caused increased unidirectional transport of glucose at the BBB in several brain regions in vivo, as determined by the doubly labeled single-pass indicator-fractionation atrial bolus injection method in anesthetized rats. We conclude that chronic hypobaric hypoxia is associated with increased glucose transport at the BBB.

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29

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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Анотація:

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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30

Hathaway, Christopher A., Caroline B. Appleyard, William H. Percy, and John L. Williams. "Experimental colitis increases blood-brain barrier permeability in rabbits." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 5 (May 1, 1999): G1174—G1180. http://dx.doi.org/10.1152/ajpgi.1999.276.5.g1174.

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Анотація:

Extraintestinal manifestations of inflammatory bowel disease are numerous. This study examined the effects of two models of acute colitis on cerebral blood flow (CBF) and permeability of the blood-brain barrier in rabbits. CBF (measured with radiolabeled microspheres), or the extraction ratio or permeability-surface area (PS) product of the blood-brain barrier to fluorescein and FITC-dextran, was measured 48 h after colitis induction with acetic acid (HAc) or trinitrobenzene sulfonic acid (TNBS). PS product for fluorescein increased ( P < 0.05) in TNBS colitis (1.33 × 10−5 ± 0.52 × 10−5 ml/s and 0.48 × 10−5 ± 0.13 × 10−5ml/s (mean ± SE) for treated ( n = 14) and untreated ( n = 10) animals, respectively. PS product for the larger FITC-dextran was not different in TNBS colitis (0.24 × 10−5 ± 0.09 × 10−5ml/s, n = 7) compared with untreated controls (0.19 × 10−5 ± 0.04 × 10−5 ml/s, n = 8). PS product for fluorescein increased ( P < 0.01) in HAc colitis compared with vehicle (2.66 × 10−5 ± 1.46 × 10−5 ml/s and 0.33 × 10−5 ± 0.05 × 10−5ml/s, respectively; n = 6 in each group). The extraction of fluorescein from the blood to the brain increased by 75% during TNBS colitis when compared with vehicle ( P < 0.05). CBF and cerebrovascular resistance did not change from the untreated control after TNBS colitis. Our data suggest that, irrespective of induction method, acute colitis increases the permeability of the blood-brain barrier to small molecules without changing CBF.

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31

Urakawa, M., K. Yamaguchi, E. Tsuchida, S. Kashiwagi, H. Ito, and T. Matsuda. "Blood-brain barrier disturbance following localized hyperthermia in rats." International Journal of Hyperthermia 11, no. 5 (January 1995): 709–18. http://dx.doi.org/10.3109/02656739509022502.

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32

Stonestreet, B. S., C. S. Patlak, K. D. Pettigrew, C. B. Reilly, and H. F. Cserr. "Ontogeny of blood-brain barrier function in ovine fetuses, lambs, and adults." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 6 (December 1, 1996): R1594—R1601. http://dx.doi.org/10.1152/ajpregu.1996.271.6.r1594.

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The ontogeny of regional blood-brain barrier function was quantified with the rate constant for influx (Ki) across the blood-brain barrier with the small molecular weight synthetic, inert hydrophilic amino acid alpha-aminoisobutyric acid (AIB) in chronically instrumented early (87 days of gestation, 60% of gestation) and late (137 days of gestation, 90% of gestation) gestation fetal, newborn (3 days of age), older (24 days of age), and adult (3 years of age) sheep. The Ki was significantly (P < 0.05) lower in the brain regions of the adult sheep and in most brain regions of newborn and older lambs compared with fetuses at 60 and 90% of gestation. The Ki exhibited regional brain heterogeneity (P < 0.05) in the five groups. The patterns of regional heterogeneity were accentuated (P < 0.05) in the younger groups. We conclude that ontogenic decreases in blood-brain barrier permeability are observed in ovine fetuses from 60% of gestation to maturity in the adult.

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33

Tennant, M., and L. D. Beazley. "A breakdown of the blood-brain barrier is associated with optic nerve regeneration in the frog." Visual Neuroscience 9, no. 2 (August 1992): 149–55. http://dx.doi.org/10.1017/s0952523800009615.

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AbstractWe have examined the integrity of the blood-brain barrier during optic nerve regeneration in the frog Liloria (Hyla) moorei using rhodamine B-labeled bovine serum albumin (RBA). A transient localized breakdown of the blood-brain barrier was observed between 1 and 5 weeks after extracranial optic nerve crush. The zone of breakdown progressed along the experimental optic nerve, ascended the opposite optic tract, and swept rostro-caudally across the tectum contralateral to the crushed nerve. By 7 weeks, the blood-brain barrier was once again intact along the length of the optic pathway. In a concurrent series of frogs, regenerating optic axons were visualized by anterograde transport of horseradish peroxidase (HRP). At each stage examined, the region reached by the front of regenerating axons corresponded to that in which the blood-brain barrier had been shown to break down.In contrast to the results after nerve crush, the blood-brain barrier remained intact along the length of the optic pathway following optic nerve ligation to prevent regeneration. We conclude that the breakdown of the blood-brain barrier which occurs during optic nerve regeneration in the frog is triggered by the regenerating axons.

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34

Reidelberger, Roger D., Dean Heimann, Linda Kelsey, and Martin Hulce. "Effects of peripheral CCK receptor blockade on feeding responses to duodenal nutrient infusions in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 2 (February 1, 2003): R389—R398. http://dx.doi.org/10.1152/ajpregu.00529.2002.

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Type A cholecystokinin receptor (CCKAR) antagonists differing in blood-brain barrier permeability were used to test the hypothesis that duodenal delivery of protein, carbohydrate, and fat produces satiety in part by an essential CCK action at CCKARs located peripheral to the blood-brain barrier. Fasted rats with open gastric fistulas received devazepide (1 mg/kg iv) or A-70104 (700 nmol · kg−1· h−1iv) and either a 30-min intravenous infusion of CCK-8 (10 nmol · kg−1· h−1) or duodenal infusion of peptone, maltose, or Intralipid beginning 10 min before 30-min access to 15% sucrose. Devazepide penetrates the blood-brain barrier; A-70104, the dicyclohexylammonium salt of Nα-3-quinolinoyl-d-Glu- N,N-dipentylamide, does not. CCK-8 inhibited sham feeding by ∼50%, and both A-70104 and devazepide abolished this response. Duodenal infusion of each of the macronutrients dose dependently inhibited sham feeding. A-70104 and devazepide attenuated inhibitory responses to each macronutrient. Thus endogenous CCK appears to act in part at CCKARs peripheral to the blood-brain barrier to inhibit food intake.

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35

Saint-Pol, Julien, Fabien Gosselet, Sophie Duban-Deweer, Gwënaël Pottiez, and Yannis Karamanos. "Targeting and Crossing the Blood-Brain Barrier with Extracellular Vesicles." Cells 9, no. 4 (April 1, 2020): 851. http://dx.doi.org/10.3390/cells9040851.

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The blood–brain barrier (BBB) is one of the most complex and selective barriers in the human organism. Its role is to protect the brain and preserve the homeostasis of the central nervous system (CNS). The central elements of this physical and physiological barrier are the endothelial cells that form a monolayer of tightly joined cells covering the brain capillaries. However, as endothelial cells regulate nutrient delivery and waste product elimination, they are very sensitive to signals sent by surrounding cells and their environment. Indeed, the neuro-vascular unit (NVU) that corresponds to the assembly of extracellular matrix, pericytes, astrocytes, oligodendrocytes, microglia and neurons have the ability to influence BBB physiology. Extracellular vesicles (EVs) play a central role in terms of communication between cells. The NVU is no exception, as each cell can produce EVs that could help in the communication between cells in short or long distances. Studies have shown that EVs are able to cross the BBB from the brain to the bloodstream as well as from the blood to the CNS. Furthermore, peripheral EVs can interact with the BBB leading to changes in the barrier’s properties. This review focuses on current knowledge and potential applications regarding EVs associated with the BBB.

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36

Thrippleton, Michael Jonathan. "MRI measurement of blood–brain barrier leakage: minding the gaps." Journal of Physiology 597, no. 3 (December 25, 2018): 667–68. http://dx.doi.org/10.1113/jp277425.

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37

HARDEBO, J. E., and J. KÅHRSTRÖM. "Endothelial negative surface charge areas and blood-brain barrier function." Acta Physiologica Scandinavica 125, no. 3 (November 1985): 495–99. http://dx.doi.org/10.1111/j.1748-1716.1985.tb07746.x.

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38

Osipova, Elena D., Oxana V. Semyachkina-Glushkovskaya, Andrey V. Morgun, Natalia V. Pisareva, Natalia A. Malinovskaya, Elizaveta B. Boitsova, Elena A. Pozhilenkova, et al. "Gliotransmitters and cytokines in the control of blood-brain barrier permeability." Reviews in the Neurosciences 29, no. 5 (July 26, 2018): 567–91. http://dx.doi.org/10.1515/revneuro-2017-0092.

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AbstractThe contribution of astrocytes and microglia to the regulation of neuroplasticity or neurovascular unit (NVU) is based on the coordinated secretion of gliotransmitters and cytokines and the release and uptake of metabolites. Blood-brain barrier (BBB) integrity and angiogenesis are influenced by perivascular cells contacting with the abluminal side of brain microvessel endothelial cells (pericytes, astrocytes) or by immune cells existing (microglia) or invading the NVU (macrophages) under pathologic conditions. The release of gliotransmitters or cytokines by activated astroglial and microglial cells is provided by distinct mechanisms, affects intercellular communication, and results in the establishment of microenvironment controlling BBB permeability and neuroinflammation. Glial glutamate transporters and connexin and pannexin hemichannels working in the tight functional coupling with the purinergic system serve as promising molecular targets for manipulating the intercellular communications that control BBB permeability in brain pathologies associated with excessive angiogenesis, cerebrovascular remodeling, and BBB-mediated neuroinflammation. Substantial progress in deciphering the molecular mechanisms underlying the (patho)physiology of perivascular glia provides promising approaches to novel clinically relevant therapies for brain disorders. The present review summarizes the current understandings on the secretory machinery expressed in glial cells (glutamate transporters, connexin and pannexin hemichannels, exocytosis mechanisms, membrane-derived microvesicles, and inflammasomes) and the role of secreted gliotransmitters and cytokines in the regulation of NVU and BBB permeability in (patho)physiologic conditions.

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39

Jezova, D. "Neuroendocrine responses and blood-brain barrier during stress." Pathophysiology 1 (November 1994): 129. http://dx.doi.org/10.1016/0928-4680(94)90280-1.

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40

Huber, Jason D., Richard D. Egleton, and Thomas P. Davis. "Molecular physiology and pathophysiology of tight junctions in the blood–brain barrier." Trends in Neurosciences 24, no. 12 (December 2001): 719–25. http://dx.doi.org/10.1016/s0166-2236(00)02004-x.

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41

Harik, Sami I. "Changes in the glucose transporter of brain capillaries." Canadian Journal of Physiology and Pharmacology 70, S1 (May 15, 1992): S113—S117. http://dx.doi.org/10.1139/y92-252.

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Brain capillary endothelium has a high density of the GLUT-1 facilitative glucose transporter protein. This is reasonable in view of the brain's high metabolic rate for glucose and its isolation behind unique capillaries with blood – brain barrier properties. Thus, the brain endothelium, which constitutes less than 0.1% of the brain weight, has to transport glucose for the much larger mass of surrounding neurons and glia. I describe here the changes that occur in the density of glucose transporters in brain capillaries of subjects with Alzheimer disease, where there is a decreased cerebral metabolic rate for glucose, and in a novel clinical entity characterized by defective glucose transport at the blood – brain barrier. In subjects with Alzheimer disease, cerebral microvessels showed a marked decrease in the density of the glucose transporter when compared with age-matched controls, but there was no change in the density of glucose transporters in erythrocyte membranes. Thus, I believe that the decreased density of glucose transporters in the brains of subjects with Alzheimer disease is the result rather than the cause of the disease. In contradistinction, the primary defect in glucose transport at the blood – brain barrier in subjects with the recently described entity is associated with decreased density of GLUT-1 in erythrocyte membranes.Key words: brain microvessels, capillary endothelium, blood – brain barrier, glucose transporter, Alzheimer disease, hypoglycorrhachia.

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42

ÖztaşL, B., and M. Küçük. "Reversible blood-brain barrier dysfunction after intracarotid hyperthermic saline infusion." International Journal of Hyperthermia 14, no. 4 (January 1998): 395–401. http://dx.doi.org/10.3109/02656739809018241.

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43

Phan, Duc TT, R. Hugh F. Bender, Jillian W. Andrejecsk, Agua Sobrino, Stephanie J. Hachey, Steven C. George, and Christopher CW Hughes. "Blood–brain barrier-on-a-chip: Microphysiological systems that capture the complexity of the blood–central nervous system interface." Experimental Biology and Medicine 242, no. 17 (February 14, 2017): 1669–78. http://dx.doi.org/10.1177/1535370217694100.

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The blood–brain barrier is a dynamic and highly organized structure that strictly regulates the molecules allowed to cross the brain vasculature into the central nervous system. The blood–brain barrier pathology has been associated with a number of central nervous system diseases, including vascular malformations, stroke/vascular dementia, Alzheimer’s disease, multiple sclerosis, and various neurological tumors including glioblastoma multiforme. There is a compelling need for representative models of this critical interface. Current research relies heavily on animal models (mostly mice) or on two-dimensional (2D) in vitro models, neither of which fully capture the complexities of the human blood–brain barrier. Physiological differences between humans and mice make translation to the clinic problematic, while monolayer cultures cannot capture the inherently three-dimensional (3D) nature of the blood–brain barrier, which includes close association of the abluminal side of the endothelium with astrocyte foot-processes and pericytes. Here we discuss the central nervous system diseases associated with blood–brain barrier pathology, recent advances in the development of novel 3D blood–brain barrier -on-a-chip systems that better mimic the physiological complexity and structure of human blood–brain barrier, and provide an outlook on how these blood–brain barrier-on-a-chip systems can be used for central nervous system disease modeling. Impact statement The field of microphysiological systems is rapidly evolving as new technologies are introduced and our understanding of organ physiology develops. In this review, we focus on Blood–Brain Barrier (BBB) models, with a particular emphasis on how they relate to neurological disorders such as Alzheimer’s disease, multiple sclerosis, stroke, cancer, and vascular malformations. We emphasize the importance of capturing the three-dimensional nature of the brain and the unique architecture of the BBB – something that until recently had not been well modeled by in vitro systems. Our hope is that this review will provide a launch pad for new ideas and methodologies that can provide us with truly physiological BBB models capable of yielding new insights into the function of this critical interface.

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44

Banks, William A. "The blood-brain barrier: Connecting the gut and the brain." Regulatory Peptides 149, no. 1-3 (August 2008): 11–14. http://dx.doi.org/10.1016/j.regpep.2007.08.027.

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45

Harris, Andrew P., Roderick Robinson, Raymond C. Koehler, Richard J. Traystman, and Christine A. Gleason. "Blood-brain barrier permeability during dopamine-induced hypertension in fetal sheep." Journal of Applied Physiology 91, no. 1 (July 1, 2001): 123–29. http://dx.doi.org/10.1152/jappl.2001.91.1.123.

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Dopamine is often used as a pressor agent in sick newborn infants, but an increase in arterial blood pressure could disrupt the blood-brain barrier (BBB), especially in the preterm newborn. Using time-dated pregnant sheep, we tested the hypothesis that dopamine-induced hypertension increases fetal BBB permeability and cerebral water content. Barrier permeability was assessed in nine brain regions, including cerebral cortex, caudate, thalamus, brain stem, cerebellum, and spinal cord, by intravenous injection of the small tracer molecule [14C]aminoisobutyric acid at 10 min after the start of dopamine or saline infusion. We studied 23 chronically catheterized fetal sheep at 0.6 (93 days, n = 10) and 0.9 (132 days, n = 13) gestation. Intravenous infusion of dopamine increased mean arterial pressure from 38 ± 3 to 53 ± 5 mmHg in 93-day fetuses and from 55 ± 5 to 77 ± 8 mmHg in 132-day fetuses without a decrease in arterial O2content. These 40% increases in arterial pressure are close to the maximum hypertension reported for physiological stresses at these ages in fetal sheep. No significant increases in the brain transfer coefficient of aminoisobutyric acid were detected in any brain region in dopamine-treated fetuses compared with saline controls at 0.6 or 0.9 gestation. There was also no significant increase in cortical water content with dopamine infusion at either age. We conclude that a 40% increase in mean arterial pressure during dopamine infusion in normoxic fetal sheep does not produce substantial BBB disruption or cerebral edema even as early as 0.6 gestation.

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46

Robinson, Peter J. "FACILITATION OF DRUG ENTRY INTO BRAIN BY OSMOTIC OPENING OF THE BLOOD-BRAIN BARRIER." Clinical and Experimental Pharmacology and Physiology 14, no. 11-12 (December 1987): 887–901. http://dx.doi.org/10.1111/j.1440-1681.1987.tb02425.x.

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47

Banks, William A., and Abba J. Kastin. "Permeability of the blood-brain barrier to melanocortins." Peptides 16, no. 6 (January 1995): 1157–61. http://dx.doi.org/10.1016/0196-9781(95)00043-j.

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48

Abbott, N. Joan. "Physiology of the blood–brain barrier and its consequences for drug transport to the brain." International Congress Series 1277 (April 2005): 3–18. http://dx.doi.org/10.1016/j.ics.2005.02.008.

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49

Fischer, H., R. Gottschlich, and A. Seelig. "Blood-Brain Barrier Permeation: Molecular Parameters Governing Passive Diffusion." Journal of Membrane Biology 165, no. 3 (October 1, 1998): 201–11. http://dx.doi.org/10.1007/s002329900434.

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50

Schlosshauer, Burkhard, and Heiko Steuer. "Comparative Anatomy, Physiology and In Vitro Models of the Blood-Brain and Blood-Retina Barrier." Current Medicinal Chemistry-Central Nervous System Agents 2, no. 3 (September 1, 2002): 175–86. http://dx.doi.org/10.2174/1568015023357978.

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