Glutamate Export at the Choroid Plexus in Health, Thiamin Deficiency, and Ethanol Intoxication: Review and Hypothesis

Introduction:  The earliest observed effect in the pathogenesis of experimental Wernicke’s encephalopathy and of ethanol intoxication in rats is impairment of the blood cerebrospinal fluid (CSF) barrier at the choroid plexus (CP). For an explanation, these observations direct attention to the role o...

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Published inAlcoholism, clinical and experimental research Vol. 32; no. 8; pp. 1339 - 1349
Main Author Nixon, Peter F.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.08.2008
Lippincott Williams & Wilkins
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Abstract Introduction:  The earliest observed effect in the pathogenesis of experimental Wernicke’s encephalopathy and of ethanol intoxication in rats is impairment of the blood cerebrospinal fluid (CSF) barrier at the choroid plexus (CP). For an explanation, these observations direct attention to the role of the CP in maintaining glutamate homeostasis in the CSF. Methods:  Characteristics of the CP epithelium (CPE) are reviewed, focusing on its role in removal of glutamate from the CSF and its potential for impairment by ethanol oxidation or by thiamin‐deficient glucose oxidation. Results:  The export of glutamate from CSF to blood at the CP is energy dependent, saturable, and stereospecific. However, the incapacity of the CP to convert glutamate to other metabolites makes it vulnerable to glutamate accumulation should α‐ketoglutarate dehydrogenase activity be decreased. Elsewhere ethanol metabolism and thiamin‐deficiency independently decrease the activity of this mitochondrial enzyme. We argue that they have the same effect within the mitochondria‐rich CPE, thereby decreasing energy production necessary for export of glutamate from CSF to blood; diverting its energy metabolism to further glutamate production; and impairing its blood CSF barrier function. This impairment appears to be mediated by glutamate and is attenuated by MK801 but whether it involves one of the CPE glutamate receptors is yet uncertain. This impairment exposes the CSF and hence the paraventricular brain extracellular fluid to neuroactive substances from the blood, including further glutamate, explaining the paraventricular location of neuropathology in Wernicke’s encephalopathy. Other organs normally protected from blood by a barrier are affected also by ethanol abuse and by thiamin deficiency, namely the eye, peripheral nerves, and the testis. Much less is known regarding the function of these barriers. Conclusions:  Impairment of the CP by ethanol intoxication and by thiamin‐deficient carbohydrate metabolism has a common, rational explanation that can guide future research.
AbstractList The earliest observed effect in the pathogenesis of experimental Wernicke's encephalopathy and of ethanol intoxication in rats is impairment of the blood cerebrospinal fluid (CSF) barrier at the choroid plexus (CP). For an explanation, these observations direct attention to the role of the CP in maintaining glutamate homeostasis in the CSF. Characteristics of the CP epithelium (CPE) are reviewed, focusing on its role in removal of glutamate from the CSF and its potential for impairment by ethanol oxidation or by thiamin-deficient glucose oxidation. The export of glutamate from CSF to blood at the CP is energy dependent, saturable, and stereospecific. However, the incapacity of the CP to convert glutamate to other metabolites makes it vulnerable to glutamate accumulation should alpha-ketoglutarate dehydrogenase activity be decreased. Elsewhere ethanol metabolism and thiamin-deficiency independently decrease the activity of this mitochondrial enzyme. We argue that they have the same effect within the mitochondria-rich CPE, thereby decreasing energy production necessary for export of glutamate from CSF to blood; diverting its energy metabolism to further glutamate production; and impairing its blood CSF barrier function. This impairment appears to be mediated by glutamate and is attenuated by MK801 but whether it involves one of the CPE glutamate receptors is yet uncertain. This impairment exposes the CSF and hence the paraventricular brain extracellular fluid to neuroactive substances from the blood, including further glutamate, explaining the paraventricular location of neuropathology in Wernicke's encephalopathy. Other organs normally protected from blood by a barrier are affected also by ethanol abuse and by thiamin deficiency, namely the eye, peripheral nerves, and the testis. Much less is known regarding the function of these barriers. Impairment of the CP by ethanol intoxication and by thiamin-deficient carbohydrate metabolism has a common, rational explanation that can guide future research.
Introduction:The earliest observed effect in the pathogenesis of experimental Wernicke's encephalopathy and of ethanol intoxication in rats is impairment of the blood cerebrospinal fluid (CSF) barrier at the choroid plexus (CP). For an explanation, these observations direct attention to the role of the CP in maintaining glutamate homeostasis in the CSF. Methods:Characteristics of the CP epithelium (CPE) are reviewed, focusing on its role in removal of glutamate from the CSF and its potential for impairment by ethanol oxidation or by thiamin-deficient glucose oxidation. Results:The export of glutamate from CSF to blood at the CP is energy dependent, saturable, and stereospecific. However, the incapacity of the CP to convert glutamate to other metabolites makes it vulnerable to glutamate accumulation should alpha -ketoglutarate dehydrogenase activity be decreased. Elsewhere ethanol metabolism and thiamin-deficiency independently decrease the activity of this mitochondrial enzyme. We argue that they have the same effect within the mitochondria-rich CPE, thereby decreasing energy production necessary for export of glutamate from CSF to blood; diverting its energy metabolism to further glutamate production; and impairing its blood CSF barrier function. This impairment appears to be mediated by glutamate and is attenuated by MK801 but whether it involves one of the CPE glutamate receptors is yet uncertain. This impairment exposes the CSF and hence the paraventricular brain extracellular fluid to neuroactive substances from the blood, including further glutamate, explaining the paraventricular location of neuropathology in Wernicke's encephalopathy. Other organs normally protected from blood by a barrier are affected also by ethanol abuse and by thiamin deficiency, namely the eye, peripheral nerves, and the testis. Much less is known regarding the function of these barriers. Conclusions:Impairment of the CP by ethanol intoxication and by thiamin-deficient carbohydrate metabolism has a common, rational explanation that can guide future research.
Introduction:  The earliest observed effect in the pathogenesis of experimental Wernicke’s encephalopathy and of ethanol intoxication in rats is impairment of the blood cerebrospinal fluid (CSF) barrier at the choroid plexus (CP). For an explanation, these observations direct attention to the role of the CP in maintaining glutamate homeostasis in the CSF. Methods:  Characteristics of the CP epithelium (CPE) are reviewed, focusing on its role in removal of glutamate from the CSF and its potential for impairment by ethanol oxidation or by thiamin‐deficient glucose oxidation. Results:  The export of glutamate from CSF to blood at the CP is energy dependent, saturable, and stereospecific. However, the incapacity of the CP to convert glutamate to other metabolites makes it vulnerable to glutamate accumulation should α‐ketoglutarate dehydrogenase activity be decreased. Elsewhere ethanol metabolism and thiamin‐deficiency independently decrease the activity of this mitochondrial enzyme. We argue that they have the same effect within the mitochondria‐rich CPE, thereby decreasing energy production necessary for export of glutamate from CSF to blood; diverting its energy metabolism to further glutamate production; and impairing its blood CSF barrier function. This impairment appears to be mediated by glutamate and is attenuated by MK801 but whether it involves one of the CPE glutamate receptors is yet uncertain. This impairment exposes the CSF and hence the paraventricular brain extracellular fluid to neuroactive substances from the blood, including further glutamate, explaining the paraventricular location of neuropathology in Wernicke’s encephalopathy. Other organs normally protected from blood by a barrier are affected also by ethanol abuse and by thiamin deficiency, namely the eye, peripheral nerves, and the testis. Much less is known regarding the function of these barriers. Conclusions:  Impairment of the CP by ethanol intoxication and by thiamin‐deficient carbohydrate metabolism has a common, rational explanation that can guide future research.
Introduction:  The earliest observed effect in the pathogenesis of experimental Wernicke’s encephalopathy and of ethanol intoxication in rats is impairment of the blood cerebrospinal fluid (CSF) barrier at the choroid plexus (CP). For an explanation, these observations direct attention to the role of the CP in maintaining glutamate homeostasis in the CSF. Methods:  Characteristics of the CP epithelium (CPE) are reviewed, focusing on its role in removal of glutamate from the CSF and its potential for impairment by ethanol oxidation or by thiamin‐deficient glucose oxidation. Results:  The export of glutamate from CSF to blood at the CP is energy dependent, saturable, and stereospecific. However, the incapacity of the CP to convert glutamate to other metabolites makes it vulnerable to glutamate accumulation should α‐ketoglutarate dehydrogenase activity be decreased. Elsewhere ethanol metabolism and thiamin‐deficiency independently decrease the activity of this mitochondrial enzyme. We argue that they have the same effect within the mitochondria‐rich CPE, thereby decreasing energy production necessary for export of glutamate from CSF to blood; diverting its energy metabolism to further glutamate production; and impairing its blood CSF barrier function. This impairment appears to be mediated by glutamate and is attenuated by MK801 but whether it involves one of the CPE glutamate receptors is yet uncertain. This impairment exposes the CSF and hence the paraventricular brain extracellular fluid to neuroactive substances from the blood, including further glutamate, explaining the paraventricular location of neuropathology in Wernicke’s encephalopathy. Other organs normally protected from blood by a barrier are affected also by ethanol abuse and by thiamin deficiency, namely the eye, peripheral nerves, and the testis. Much less is known regarding the function of these barriers. Conclusions:  Impairment of the CP by ethanol intoxication and by thiamin‐deficient carbohydrate metabolism has a common, rational explanation that can guide future research.
Author Nixon, Peter F.
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Issue 8
Keywords Choroid plexus
Testis
Peripheral nerve
Peripheral Nerves
Central nervous system
B-Vitamins
Glutamate receptor
Review
Testicle
Hypothesis
Eye
Visual system
Alcoholic beverage
Glutamate Receptors
Thiamin Deficiency
Thiamine
Ependymal organ
Ethanol
Health
Deficiency
Glutamate
Male genital system
Ethanol Intoxication
Glutamate Transport
Review and Hypothesis
Excitatory aminoacid
Neurotransmitter
Poisoning
Transport
Bibliographic review
Language English
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PublicationTitle Alcoholism, clinical and experimental research
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1997; 102
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Snippet Introduction:  The earliest observed effect in the pathogenesis of experimental Wernicke’s encephalopathy and of ethanol intoxication in rats is impairment of...
The earliest observed effect in the pathogenesis of experimental Wernicke's encephalopathy and of ethanol intoxication in rats is impairment of the blood...
Introduction:  The earliest observed effect in the pathogenesis of experimental Wernicke’s encephalopathy and of ethanol intoxication in rats is impairment of...
Introduction:The earliest observed effect in the pathogenesis of experimental Wernicke's encephalopathy and of ethanol intoxication in rats is impairment of...
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SubjectTerms Alcoholic Intoxication - metabolism
Alcoholism and acute alcohol poisoning
Animals
Biological and medical sciences
Choroid Plexus
Choroid Plexus - metabolism
Disease Models, Animal
Ethanol - metabolism
Ethanol Intoxication
Eye
Glucose - metabolism
Glutamate Receptors
Glutamate Transport
Glutamates - blood
Glutamates - cerebrospinal fluid
Glutamates - metabolism
Humans
Medical sciences
Peripheral Nerves
Rats
Review and Hypothesis
Testis
Thiamin Deficiency
Thiamine Deficiency - metabolism
Toxicology
Title Glutamate Export at the Choroid Plexus in Health, Thiamin Deficiency, and Ethanol Intoxication: Review and Hypothesis
URI https://api.istex.fr/ark:/67375/WNG-NFCRMV6H-G/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1530-0277.2008.00727.x
https://www.ncbi.nlm.nih.gov/pubmed/18616670
https://search.proquest.com/docview/21052410
Volume 32
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