PUBLICATION

Short exposure to low concentrations of alcohol during embryonic development has only subtle and strain- dependent effect on the levels of five amino acid neurotransmitters in zebrafish

Authors
Mahabir, S., Chatterjee, D., Gerlai, R.
ID
ZDB-PUB-180611-4
Date
2018
Source
Neurotoxicology and teratology   68: 91-96 (Journal)
Registered Authors
Gerlai, Robert T.
Keywords
Aspartate, Embryonic alcohol, Ethanol, FASD, GABA, Glutamate, Glycine, Taurine, Zebrafish
MeSH Terms
  • Animals
  • Aspartic Acid/metabolism
  • Brain/metabolism*
  • Dose-Response Relationship, Drug
  • Embryo, Nonmammalian/drug effects
  • Ethanol/toxicity*
  • Glutamic Acid/metabolism
  • Glycine/metabolism
  • Species Specificity*
  • Taurine/metabolism
  • Zebrafish*
  • gamma-Aminobutyric Acid/metabolism
PubMed
29886245 Full text @ Neurotoxicol. Teratol.
Abstract
The zebrafish has been successfully employed to model and study the effects of embryonic alcohol exposure. Short exposure to low alcohol concentrations during embryonic development has been shown to significantly disrupt social behavior as well as the dopaminergic and serotoninergic systems in zebrafish. However, analysis of potential effects of embryonic alcohol exposure on other amino acid neurotransmitter systems has not been performed. Here we analyzed neurochemicals obtained from adult AB and TU strain zebrafish that were immersed in 0.00% (control), 0.25%, 0.50%, 0.75% or 1.00% alcohol solution (vol/vol%) at 24 h post-fertilization for 2 h. From whole brain extracts, we quantified glutamate, aspartate, glycine, taurine and GABA levels using high performance liquid chromatography (HPLC). We found embryonic alcohol exposure not to have any significant effect on the levels of glutamate, aspartate, glycine and GABA in both AB and TU zebrafish. AB zebrafish showed a significant elevation of taurine levels, but only in the highest alcohol dose group compared to control. These results, albeit mainly negative, together with prior findings suggest that behavioral abnormalities resulting from embryonic alcohol exposure described before for AB zebrafish may primarily be due to altered dopaminergic and serotoninergic mechanisms. Furthermore, a Principal Component Analysis conducted with all neurochemicals tested in this and in our prior study, found a strain-dependent correlation structure response to embryonic alcohol treatment, confirming that embryonic alcohol effects may be genotype dependent.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping