Ethanol and voltage- or receptor-mediated increases in cytosolic Ca2+ in brain cells

Jo Ellen Dildy-Mayfield, Tina Machu, Steven W. Leslie

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20 Scopus citations

Abstract

Dissociated brain cells were isolated from newborn rat pups and loaded with fura-2. Different mechanisms for stimulating increased free intracellular Ca2+ concentrations ([Ca2+]i) were examined in the absence and presence of ethanol. KCl, carbachol, and kainate concentration-dependently increased [Ca2+]i. Quisqualate also elevated [Ca2+]i but did not produce clear concentration-dependent increases. KCl, carbachol, and quisqualate responses reached peak levels within 10-30 s and then desensitized within 90 s. However, kainate-stimulated increases in [Ca2+]i plateaued and did not decline after 90 s. Of these different [Ca2+]i-mediated processes, only 60 mM KCl stimulation was significantly inhibited by 100 mM ethanol, while lower KCl concentrations were not affected. Carbachol-induced release of intracellular Ca2+ and activation of non-NMDA (i.e., kainate, quisqualate) excitatory amino acid receptor-operated cation channels were also not significantly inhibited by 100 mM ethanol. Thus, in acutely dissociated brain cells from newborn rats, only Ca2+ influx via voltage- and, as reported previously, NMDA-operated Ca2+ channels were sensitive to ethanol inhibition.

Original languageEnglish
Pages (from-to)63-69
Number of pages7
JournalAlcohol
Volume9
Issue number1
DOIs
StatePublished - 1992

Keywords

  • Carbachol
  • Ethanol
  • Excitatory amino acid receptor-operated channels
  • Free intracellular Ca
  • Fura-2
  • Kainate
  • Neonatal dissociated brain cells
  • Quisqualate
  • Voltage-dependent Ca channels

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