Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

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

T A McIntyre1, M G Souder, M W Hartl

  • 1Department of Chemistry, Penn State Berks-Lehigh Valley College, P.O. Box 7009, Reading, PA, USA.

Brain Research. Developmental Brain Research
|November 24, 1999
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Prediction of animal clearance using naïve Bayesian classification and extended connectivity fingerprints.

Xenobiotica; the fate of foreign compounds in biological systems·2009
Same author

Differences in the total body clearance of lead compounds in the rat and mouse: impact on pharmacokinetic screening strategy.

Xenobiotica; the fate of foreign compounds in biological systems·2008
Same author

Differential expression of glucose transporters during chick embryogenesis.

Cellular and molecular life sciences : CMLS·2001
Same author

Increased intracellular localization of brain GLUT-1 transporter in response to ethanol during chick embryogenesis.

The American journal of physiology·1999
Same author

Experimental models used to measure direct and indirect ethanol teratogenicity.

Alcohol and alcoholism (Oxford, Oxfordshire)·1999
Same author

Sodium ion-dependent (N-methylamino)-alpha-isobutyric [correction of isobutryic] acid uptake by embryonic chick cells exposed to ethanol in ovo:response to the stimulation/downregulation of protein kinases.

Alcohol and alcoholism (Oxford, Oxfordshire)·1998
Same journal

Postnatal development of GFAP, connexin43 and connexin30 in cat visual cortex.

Brain research. Developmental brain research·2005
Same journal

Expression of gamma-aminobutyric acid B receptor subunits in hypothalamus of male and female developing rats.

Brain research. Developmental brain research·2005
Same journal

Retinal neurospheres prepared as tissue for transplantation.

Brain research. Developmental brain research·2005
Same journal

Effects of prenatal stress on anxiety and social interactions in adult rats.

Brain research. Developmental brain research·2005
Same journal

Disruption of cerebellar granule cell development in the Pax6 mutant, Sey mouse.

Brain research. Developmental brain research·2005
Same journal

Cytoskeletal, synaptic, and nuclear protein changes associated with rat interface organotypic hippocampal slice culture development.

Brain research. Developmental brain research·2005
See all related articles

Prenatal ethanol exposure, a cause of fetal alcohol syndrome (FAS), affects chick brain development. Ethanol exposure decreases expression of specific protein kinase C (PKC) isoforms crucial for growth.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Pharmacology

Background:

  • Prenatal ethanol exposure is a leading cause of birth defects, collectively known as fetal alcohol syndrome (FAS).
  • Protein kinase C (PKC) plays a critical role in cell cycle regulation and cellular growth.
  • Understanding ethanol's impact on PKC expression is vital for elucidating FAS mechanisms.

Purpose of the Study:

  • To investigate the effects of ethanol on the expression of various protein kinase C (PKC) isoforms in the developing chick brain.
  • To determine which PKC isoforms are developmentally regulated in the embryonic chick brain.
  • To correlate ethanol-induced growth deficits with changes in PKC isoform expression.

Main Methods:

  • Chick embryos were exposed to varying doses of ethanol.

Related Experiment Videos

  • Head and brain weights were measured at embryonic days 5, 7, and 10.
  • Western blot analysis using isoform-specific antibodies was performed to quantify PKC-alpha, -beta, -gamma, -delta, -epsilon, -iota, -lambda, -mu, and -zeta expression.

    • Main Results:

    • Ethanol exposure led to a dose-dependent decrease in chick head weight by day 5 and brain weight by days 7 and 10.
    • Only PKC-alpha, -gamma, -epsilon, and -iota isoforms were expressed in the developing chick brain before day 10.
    • Ethanol significantly decreased the expression of PKC-alpha (days 5, 7, 10), PKC-gamma (days 7, 10), and PKC-epsilon (day 7), while PKC-iota expression remained unaffected.

    Conclusions:

    • Specific PKC isoforms (alpha, gamma, epsilon) are developmentally regulated in the embryonic chick brain.
    • Ethanol exposure during development inhibits the expression of these developmentally regulated PKC isoforms.
    • These findings suggest a potential mechanism by which prenatal ethanol exposure disrupts embryonic brain growth and development.