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

Timothy Othman, Christopher J.D. Sinclair, Norman Haughey, Jonathan D. Geiger, Fiona E. Parkinson

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish (US)
Article number373358
Pages (from-to)289-296
Number of pages8
JournalNeurochemical Research
Issue number4
StatePublished - 2002
Externally publishedYes


  • Adenosine
  • Astrocytes
  • Ethanol
  • Glutamate transporters
  • Nucleoside transporters
  • Protein kinase C

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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