La maladie de Parkinson au Canada (serveur d'exploration)

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Ethanol alters glutamate but not adenosine uptake in rat astrocytes: evidence for protein kinase C involvement.

Identifieur interne : 002F77 ( Main/Exploration ); précédent : 002F76; suivant : 002F78

Ethanol alters glutamate but not adenosine uptake in rat astrocytes: evidence for protein kinase C involvement.

Auteurs : Timothy Othman [Canada] ; Christopher J D. Sinclair ; Norman Haughey ; Jonathan D. Geiger ; Fiona E. Parkinson

Source :

RBID : pubmed:11958530

English descriptors

Abstract

Glutamate is the primary excitatory neurotransmitter in brain. By stimulating neuronal activity, glutamate increases cellular energy utilization, enhances ATP hydrolysis and promotes the formation of adenosine. Adenosine has receptor-mediated effects that reduce or oppose the excitatory effects of glutamate. As a possible mechanism for ethanol's ability to inhibit excitatory effects of glutamate and enhance inhibitory effects of adenosine, we tested the hypothesis that ethanol promotes [3H]glutamate uptake and inhibits [3H]adenosine uptake. Using primary cultures of rat astrocytes, we found that acute treatment with ethanol (50 mM, 30 min) inhibited [3H]glutamate uptake and reduced protein kinase C (PKC)-induced stimulation of [3H]glutamate uptake. Prolonged treatment (50 mM, 3 day) with ethanol, however, increased both [3H]glutamate uptake and PKC activity. Contrary to other cell types, neither acute or chronic ethanol exposure affected [3H]adenosine uptake in astrocytes. These data indicate that in rat cortical astrocytes ethanol affects [3H]glutamate uptake but not [3H]adenosine uptake by affecting PKC modulation of transporter activity.

PubMed: 11958530


Affiliations:


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Le document en format XML

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<term>Adenosine (metabolism)</term>
<term>Adenosine Triphosphate (metabolism)</term>
<term>Alkaloids</term>
<term>Animals</term>
<term>Astrocytes (drug effects)</term>
<term>Astrocytes (metabolism)</term>
<term>Benzophenanthridines</term>
<term>Biological Transport (drug effects)</term>
<term>Cells, Cultured</term>
<term>Cerebral Cortex (drug effects)</term>
<term>Cerebral Cortex (embryology)</term>
<term>Cerebral Cortex (metabolism)</term>
<term>Embryo, Mammalian</term>
<term>Ethanol (pharmacology)</term>
<term>Glutamic Acid (metabolism)</term>
<term>Kinetics</term>
<term>Phenanthridines (pharmacology)</term>
<term>Protein Kinase C (metabolism)</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Reverse Transcriptase Polymerase Chain Reaction</term>
<term>Tetradecanoylphorbol Acetate (pharmacology)</term>
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<div type="abstract" xml:lang="en">Glutamate is the primary excitatory neurotransmitter in brain. By stimulating neuronal activity, glutamate increases cellular energy utilization, enhances ATP hydrolysis and promotes the formation of adenosine. Adenosine has receptor-mediated effects that reduce or oppose the excitatory effects of glutamate. As a possible mechanism for ethanol's ability to inhibit excitatory effects of glutamate and enhance inhibitory effects of adenosine, we tested the hypothesis that ethanol promotes [3H]glutamate uptake and inhibits [3H]adenosine uptake. Using primary cultures of rat astrocytes, we found that acute treatment with ethanol (50 mM, 30 min) inhibited [3H]glutamate uptake and reduced protein kinase C (PKC)-induced stimulation of [3H]glutamate uptake. Prolonged treatment (50 mM, 3 day) with ethanol, however, increased both [3H]glutamate uptake and PKC activity. Contrary to other cell types, neither acute or chronic ethanol exposure affected [3H]adenosine uptake in astrocytes. These data indicate that in rat cortical astrocytes ethanol affects [3H]glutamate uptake but not [3H]adenosine uptake by affecting PKC modulation of transporter activity.</div>
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