Choroid Plexus Dysfunction: The Initial Event in the Pathogenesis of Wernicke's Encephalopathy and Ethanol Intoxication
Background: In both acute ethanol intoxication and in thiamin deficient glucose metabolism, previous studies have detected blood‐brain barrier (BBB) and/or blood‐CSF‐barrier (BCSFB) impairment but were unable to assess their significance in relation to other changes in the brain. Methods: Contrast...
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Published in | Alcoholism, clinical and experimental research Vol. 32; no. 8; pp. 1513 - 1523 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.08.2008
Lippincott Williams & Wilkins |
Subjects | |
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Abstract | Background: In both acute ethanol intoxication and in thiamin deficient glucose metabolism, previous studies have detected blood‐brain barrier (BBB) and/or blood‐CSF‐barrier (BCSFB) impairment but were unable to assess their significance in relation to other changes in the brain.
Methods: Contrast‐enhanced, magnetic resonance imaging (MRI) was used to detect and time any impairment of the BBB or BCSFB in rats given an acute ethanol load or in rats made thiamin deficient to the point of mild ataxia and then given an acute glucose load.
Results: The BCSFB at the choroid plexus (CP) was impaired within 10 minutes by either (i) a single i.p. dose of glucose in thiamin‐deficiency, an effect that was attenuated by prior MK801 and preceded the published onset of exacerbation of motor incoordination and elevation of brain glutamate derivatives; or (ii) a single i.p. dose of ethanol in thiamin‐sufficiency, an effect that was proportional to the blood alcohol concentration and preceded the published onset of signs of intoxication. In contrast to the BCSFB, the BBB remained intact throughout the 90 minutes period of these experiments.
Conclusions: In both ethanol intoxication and thiamin‐deficient glucose metabolism, BCSFB impairment exposes the CSF and hence the brain extracellular fluid to neuroactive substances from the blood. CP impairment is the earliest detected event in both these animal models; and explains the paraventricular location of WE neuropathology and why WE is associated with, but not dependent on, alcoholism. |
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AbstractList | In both acute ethanol intoxication and in thiamin deficient glucose metabolism, previous studies have detected blood-brain barrier (BBB) and/or blood-CSF-barrier (BCSFB) impairment but were unable to assess their significance in relation to other changes in the brain.
Contrast-enhanced, magnetic resonance imaging (MRI) was used to detect and time any impairment of the BBB or BCSFB in rats given an acute ethanol load or in rats made thiamin deficient to the point of mild ataxia and then given an acute glucose load.
The BCSFB at the choroid plexus (CP) was impaired within 10 minutes by either (i) a single i.p. dose of glucose in thiamin-deficiency, an effect that was attenuated by prior MK801 and preceded the published onset of exacerbation of motor incoordination and elevation of brain glutamate derivatives; or (ii) a single i.p. dose of ethanol in thiamin-sufficiency, an effect that was proportional to the blood alcohol concentration and preceded the published onset of signs of intoxication. In contrast to the BCSFB, the BBB remained intact throughout the 90 minutes period of these experiments.
In both ethanol intoxication and thiamin-deficient glucose metabolism, BCSFB impairment exposes the CSF and hence the brain extracellular fluid to neuroactive substances from the blood. CP impairment is the earliest detected event in both these animal models; and explains the paraventricular location of WE neuropathology and why WE is associated with, but not dependent on, alcoholism. Background: In both acute ethanol intoxication and in thiamin deficient glucose metabolism, previous studies have detected blood‐brain barrier (BBB) and/or blood‐CSF‐barrier (BCSFB) impairment but were unable to assess their significance in relation to other changes in the brain. Methods: Contrast‐enhanced, magnetic resonance imaging (MRI) was used to detect and time any impairment of the BBB or BCSFB in rats given an acute ethanol load or in rats made thiamin deficient to the point of mild ataxia and then given an acute glucose load. Results: The BCSFB at the choroid plexus (CP) was impaired within 10 minutes by either (i) a single i.p. dose of glucose in thiamin‐deficiency, an effect that was attenuated by prior MK801 and preceded the published onset of exacerbation of motor incoordination and elevation of brain glutamate derivatives; or (ii) a single i.p. dose of ethanol in thiamin‐sufficiency, an effect that was proportional to the blood alcohol concentration and preceded the published onset of signs of intoxication. In contrast to the BCSFB, the BBB remained intact throughout the 90 minutes period of these experiments. Conclusions: In both ethanol intoxication and thiamin‐deficient glucose metabolism, BCSFB impairment exposes the CSF and hence the brain extracellular fluid to neuroactive substances from the blood. CP impairment is the earliest detected event in both these animal models; and explains the paraventricular location of WE neuropathology and why WE is associated with, but not dependent on, alcoholism. Background: In both acute ethanol intoxication and in thiamin deficient glucose metabolism, previous studies have detected blood‐brain barrier (BBB) and/or blood‐CSF‐barrier (BCSFB) impairment but were unable to assess their significance in relation to other changes in the brain. Methods: Contrast‐enhanced, magnetic resonance imaging (MRI) was used to detect and time any impairment of the BBB or BCSFB in rats given an acute ethanol load or in rats made thiamin deficient to the point of mild ataxia and then given an acute glucose load. Results: The BCSFB at the choroid plexus (CP) was impaired within 10 minutes by either (i) a single i.p. dose of glucose in thiamin‐deficiency, an effect that was attenuated by prior MK801 and preceded the published onset of exacerbation of motor incoordination and elevation of brain glutamate derivatives; or (ii) a single i.p. dose of ethanol in thiamin‐sufficiency, an effect that was proportional to the blood alcohol concentration and preceded the published onset of signs of intoxication. In contrast to the BCSFB, the BBB remained intact throughout the 90 minutes period of these experiments. Conclusions: In both ethanol intoxication and thiamin‐deficient glucose metabolism, BCSFB impairment exposes the CSF and hence the brain extracellular fluid to neuroactive substances from the blood. CP impairment is the earliest detected event in both these animal models; and explains the paraventricular location of WE neuropathology and why WE is associated with, but not dependent on, alcoholism. Background:In both acute ethanol intoxication and in thiamin deficient glucose metabolism, previous studies have detected blood-brain barrier (BBB) and-or blood-CSF-barrier (BCSFB) impairment but were unable to assess their significance in relation to other changes in the brain. Methods:Contrast-enhanced, magnetic resonance imaging (MRI) was used to detect and time any impairment of the BBB or BCSFB in rats given an acute ethanol load or in rats made thiamin deficient to the point of mild ataxia and then given an acute glucose load. Results:The BCSFB at the choroid plexus (CP) was impaired within 10minutes by either (i) a single i.p. dose of glucose in thiamin-deficiency, an effect that was attenuated by prior MK801 and preceded the published onset of exacerbation of motor incoordination and elevation of brain glutamate derivatives; or (ii) a single i.p. dose of ethanol in thiamin-sufficiency, an effect that was proportional to the blood alcohol concentration and preceded the published onset of signs of intoxication. In contrast to the BCSFB, the BBB remained intact throughout the 90minutes period of these experiments. Conclusions:In both ethanol intoxication and thiamin-deficient glucose metabolism, BCSFB impairment exposes the CSF and hence the brain extracellular fluid to neuroactive substances from the blood. CP impairment is the earliest detected event in both these animal models; and explains the paraventricular location of WE neuropathology and why WE is associated with, but not dependent on, alcoholism. |
Author | Zelaya, Fernando Nixon, Peter F. Rose, Stephen E. Jordan, Lindsay Zimitat, Craig |
Author_xml | – sequence: 1 givenname: Peter F. surname: Nixon fullname: Nixon, Peter F. organization: From the Department of Biochemistry and Molecular Biology (PFN, LJ, CZ) and Centre for Magnetic Resonance (SER, FZ), The University of Queensland, St Lucia, Queensland, Australia – sequence: 2 givenname: Lindsay surname: Jordan fullname: Jordan, Lindsay – sequence: 3 givenname: Craig surname: Zimitat fullname: Zimitat, Craig – sequence: 4 givenname: Stephen E. surname: Rose fullname: Rose, Stephen E. organization: From the Department of Biochemistry and Molecular Biology (PFN, LJ, CZ) and Centre for Magnetic Resonance (SER, FZ), The University of Queensland, St Lucia, Queensland, Australia – sequence: 5 givenname: Fernando surname: Zelaya fullname: Zelaya, Fernando |
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Keywords | Choroid plexus Rat Pathogenesis Central nervous system B-Vitamins Alcoholic beverage Encephalopathy Thiamin Deficiency Thiamine Contrast-Enhanced MRI Ependymal organ Nervous system diseases Ethanol Deficiency Rodentia Wernicke's Encephalopathy Contrast Nuclear magnetic resonance imaging Cerebral disorder Ethanol Intoxication Vertebrata Mammalia Dysfunction Animal Central nervous system disease Poisoning |
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Snippet | Background: In both acute ethanol intoxication and in thiamin deficient glucose metabolism, previous studies have detected blood‐brain barrier (BBB) and/or... In both acute ethanol intoxication and in thiamin deficient glucose metabolism, previous studies have detected blood-brain barrier (BBB) and/or... Background: In both acute ethanol intoxication and in thiamin deficient glucose metabolism, previous studies have detected blood‐brain barrier (BBB) and/or... Background:In both acute ethanol intoxication and in thiamin deficient glucose metabolism, previous studies have detected blood-brain barrier (BBB) and-or... |
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SubjectTerms | Alcoholic Intoxication - etiology Alcoholic Intoxication - physiopathology Alcoholism and acute alcohol poisoning Animals Biological and medical sciences Blood-Brain Barrier - drug effects Central Nervous System Depressants - pharmacology Choroid Plexus Choroid Plexus - drug effects Choroid Plexus - pathology Choroid Plexus - physiopathology Contrast-Enhanced MRI Disease Models, Animal Dizocilpine Maleate - pharmacology Dose-Response Relationship, Drug Ethanol - pharmacology Ethanol Intoxication Female Glucose - metabolism Glucose - pharmacology Magnetic Resonance Imaging Medical sciences Neuroprotective Agents - pharmacology Rat Rats Rats, Wistar Thiamin Deficiency Thiamine Deficiency - metabolism Toxicology Wernicke Encephalopathy - etiology Wernicke Encephalopathy - physiopathology Wernicke's Encephalopathy |
Title | Choroid Plexus Dysfunction: The Initial Event in the Pathogenesis of Wernicke's Encephalopathy and Ethanol Intoxication |
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