1
40
3
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.brainres.2011.10.005" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.brainres.2011.10.005</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
155-163
Volume
1425
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Neuroprotective Effects Of Bilobalide Are Accompanied By A Reduction Of Ischemia-induced Glutamate Release In Vivo
Publisher
An entity responsible for making the resource available
Brain Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-11
Subject
The topic of the resource
brain-injury; cerebral-artery occlusion; extract egb-761; Ginkgo biloba; Ginkgo biloba; Glucose; inhibition; mice; Microdialysis; Microdialysis; Middle cerebral artery occlusion; Neurosciences & Neurology; phospholipid breakdown; sensorimotor; stroke; stroke
Creator
An entity primarily responsible for making the resource
Lang D; Kiewert C; Mdzinarishvili A; Schwarzkopf T M; Sumbria R; Hartmann J; Klein J
Description
An account of the resource
Neuroprotective properties of bilobalide, a specific constituent of Ginkgo extracts, were tested in a mouse model of stroke. After 24 h of middle cerebral artery occlusion (MCAO), bilobalide reduced infarct areas in the core region (striatum) by 40-50% when given at 10 mg/kg 1 h prior to MCAO. Neuroprotection was also observed at lower doses, or when the drug was given 1 h past stroke induction. Sensorimotor function in mice was improved by bilobalide as shown by corner and chimney tests. When brain metabolism in situ was monitored by microdialysis, MCAO caused a rapid disappearance of extracellular glucose in the striatum which returned to baseline levels after reperfusion. Extracellular levels of glutamate were increased by more than ten-fold in striatal tissue, and by four- to fivefold in hippocampal tissue (penumbra). Bilobalide did not affect glucose levels but strongly attenuated glutamate release in both core and penumbra regions. Bilobalide was equally active when given locally via the microdialysis probe and also reduced ischemia-induced glutamate release in vitro in brain slices. We conclude that bilobalide is a strong neuroprotectant in vivo at doses that can be used therapeutically in humans. The mechanism of action evidently involves reduction of glutamate release, thereby reducing excitotoxicity. (C) 2011 Elsevier B.V. All rights reserved.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.brainres.2011.10.005" target="_blank" rel="noreferrer noopener">10.1016/j.brainres.2011.10.005</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2011
Brain research
brain-injury
cerebral-artery occlusion
extract egb-761
Ginkgo Biloba
GLUCOSE
Hartmann J
inhibition
Journal Article or Conference Abstract Publication
Kiewert C
Klein J
Lang D
Mdzinarishvili A
Mice
Microdialysis
Middle cerebral artery occlusion
Neurosciences & Neurology
phospholipid breakdown
Schwarzkopf T M
Sensorimotor
stroke
Sumbria R
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.brainres.2009.11.068" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.brainres.2009.11.068</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
101-107
Volume
1312
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Metabolic And Transmitter Changes In Core And Penumbra After Middle Cerebral Artery Occlusion In Mice
Publisher
An entity responsible for making the resource available
Brain Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-02
Subject
The topic of the resource
acetylcholine; Choline; focal ischemia; Glucose; glutamate; glutamate; Glycerol; hippocampus; hippocampus; intracerebral microdialysis; Microdialysis; mutant mice; neurodegenerative disorders; Neurosciences & Neurology; rat; release; reperfusion; Striatum; stroke
Creator
An entity primarily responsible for making the resource
Kiewert C; Mdzinarishvili A; Hartmann J; Bickel U; Klein J
Description
An account of the resource
Middle cerebral artery occlusion (MCAO) is a popular model in experimental stroke research and causes prominent ischemic damage in the forebrain. To characterize metabolic changes induced by MCAO, we have induced permanent MCAO in mice that were implanted with a microdialysis probe in either striatum or hippocampus. Immediately after the onset of ischemia, glucose levels dropped to <10% of basal values in the striatum while they dropped to 50%, and recovered thereafter, in hippocampus. Extracellular levels of glutamate rose 80-fold in the striatum but only 10-fold, and in a transient fashion, in hippocampus. In striatum, release of acetylcholine briefly increased, then dropped to very low values. Both glycerol and choline levels increased strongly during ischemia in the striatum reflecting membrane breakdown. In hippocampus, glycerol increased transiently while the increase of choline levels was moderate. Taken together, these observations delineate metabolic changes in ischemic mouse brain with the striatum representing the core area of ischemia. In comparison, the dorsal hippocampus was identified as a brain area suitable for monitoring metabolic responses in the penumbra region. (C) 2009 Elsevier B.V. All rights reserved.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.brainres.2009.11.068" target="_blank" rel="noreferrer noopener">10.1016/j.brainres.2009.11.068</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2010
Acetylcholine
Bickel U
Brain research
Choline
focal ischemia
GLUCOSE
glutamate
Glycerol
Hartmann J
Hippocampus
intracerebral microdialysis
Journal Article or Conference Abstract Publication
Kiewert C
Klein J
Mdzinarishvili A
Microdialysis
mutant mice
neurodegenerative disorders
Neurosciences & Neurology
rat
release
Reperfusion
striatum
stroke
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1124/jpet.109.157776" target="_blank" rel="noreferrer noopener">http://doi.org/10.1124/jpet.109.157776</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
371-379
Issue
2
Volume
332
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Nicotine Exacerbates Brain Edema during In Vitro and In Vivo Focal Ischemic Conditions
Publisher
An entity responsible for making the resource available
Journal of Pharmacology and Experimental Therapeutics
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-02
Subject
The topic of the resource
acetylcholine-receptor subtypes; barrier; cigarette-smoking; exposure; middle cerebral-artery; occlusion; permeability; Pharmacology & Pharmacy; rat; risk; stroke; water
Creator
An entity primarily responsible for making the resource
Paulson J R; Yang T Z; Selvaraj P K; Mdzinarishvili A; Van der Schyf C J; Klein J; Bickel U; Abbruscato T J
Description
An account of the resource
We have previously shown that nicotine, the addictive component of tobacco products, alters the blood-brain barrier (BBB) Na+, K+, 2Cl(-) cotransporter (NKCC) during in vitro hypoxia-aglycemia exposure. Attenuation of abluminal NKCC suggests that accumulation of ions in the brain extracellular fluid would result in an increase of fluid or cytotoxic edema in the brain during hypoxia-aglycemia or stroke conditions. To further investigate whether nicotine products have the potential to worsen stroke outcome by increasing edema formation, two separate models to mimic stroke conditions were utilized to decipher the effects of short-term and long-term administrations of nicotine products on brain edema following stroke. Oxygen glucose deprivation (OGD) was studied in rat hippocampal slices with short-term or long-term exposure to nicotine and cigarette smoke constituents. During short-term exposure, the presence of nicotine at a concentration mimicking heavy smokers increased water content of hippocampal slices during OGD. Furthermore, long-term 1-week administration of nicotine increased water content in hippocampal slices that could be attenuated with nicotine acetylcholine receptor (nAChR) antagonists, suggesting nicotine increase edema during OGD via nAChRs. A second model of focal ischemia, middle cerebral artery occlusion, showed an increase of infarct size during short-term exposure to nicotine and an increase of edema during both short-term and long-term administration of nicotine, compared with saline controls. These findings support the paradigm that nicotine products not only increase the incidence of stroke but also have the potential to worsen stroke outcome by increased edema formation.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1124/jpet.109.157776" target="_blank" rel="noreferrer noopener">10.1124/jpet.109.157776</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2010
Abbruscato T J
acetylcholine-receptor subtypes
barrier
Bickel U
cigarette-smoking
exposure
Journal Article
Journal of Pharmacology and Experimental Therapeutics
Klein J
Mdzinarishvili A
middle cerebral-artery
occlusion
Paulson J R
Permeability
Pharmacology & Pharmacy
rat
Risk
Selvaraj P K
stroke
Van der Schyf C J
Water
Yang T Z