Ethanol-induced decrease of developmental PKC isoform expression in the embryonic chick brain

Timothy A. McIntyre, Matthew G. Souder, Michael W. Hartl, Ivan A. Shibley

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


Prenatal ethanol exposure can cause a number of physiological deficits known as fetal alcohol syndrome (FAS). Because protein kinase C (PKC) regulates the cell cycle and has been linked to growth, we examined the effect of ethanol on PKC isoform expression in a developing chick brain. Ethanol exposure causes decreased head weight in chickens at day 5 in a dose-dependent manner and a decreased brain weight at days 7 and 10 at an ethanol concentration of 1.0 g/kg. Antibodies specific for PKC-α, β, γ, δ, ε, ι, λ, μ and ζ were used to examine ethanol's effect on PKC expression in the growth-suppressed brain at days 5, 7 and 10 of development. Only four of the PKC isoforms tested are expressed in the chick brain prior to day 10: α, γ, ε, and ι. PKC-α, γ, and ε are developmentally increased during the time period studied. Ethanol causes a decreased expression of PKC-α on days 5, 7 and 10 and a decreased expression of PKC-γ on days 7 and 10. Ethanol causes a decreased expression of PKC-ε only on day 7. PKC-ι expression is unchanged over the developmental times studied and ethanol exposure has no effect on PKC-ι expression. These data suggest that only specific PKC isoforms are developmentally expressed in the embryonic chick brain and that ethanol may inhibit the expression of those PKC isoforms that are developmentally regulated. Copyright (C) 1999 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)191-197
Number of pages7
JournalDevelopmental Brain Research
Issue number2
StatePublished - Nov 18 1999

All Science Journal Classification (ASJC) codes

  • Developmental Neuroscience
  • Developmental Biology


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