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

37 Scopus citations


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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