| Autor: | Timothy Othman, Christopher J. D. Sinclair, Norman J. Haughey, Jonathan D. Geiger, Fiona E. Parkinson |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
medicine.medical_specialty
Glutamate receptor General Medicine Biology Biochemistry Adenosine Cellular and Molecular Neuroscience chemistry.chemical_compound Endocrinology medicine.anatomical_structure chemistry ATP hydrolysis Metabotropic glutamate receptor Internal medicine medicine Neuroglia Neurotransmitter Protein kinase C Astrocyte medicine.drug |
| Zdroj: | Neurochemical Research. 27:289-296 |
| ISSN: | 0364-3190 |
| DOI: | 10.1023/a:1014955111742 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
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