PMID- 12457071
OWN - NLM
STAT- MEDLINE
DCOM- 20030317
LR  - 20171101
IS  - 0378-5866 (Print)
IS  - 0378-5866 (Linking)
VI  - 24
IP  - 4
DP  - 2002
TI  - Hindbrain and cranial nerve dysmorphogenesis result from acute maternal ethanol 
      administration.
PG  - 328-42
AB  - Acute exposure of mouse embryos to ethanol during stages of hindbrain 
      segmentation results in excessive cell death in specific cell populations. This 
      study details the ethanol-induced cell loss and defines the subsequent effects of 
      this early insult on rhombomere and cranial nerve development. Ethanol at a 
      teratogenic dosage (2.9 g/kg) or a comparable volume of vehicle was administered 
      in each of two intraperitoneal injections to pregnant C57BL/6J mice on 
      gestational day (GD) 8, 8 h, and GD 8, 12 h (defined hereafter as GD 8.5). 
      Ethanol-exposed GD 9 embryos, visualized in three dimensions using laser scanning 
      confocal microscopy of LysoTracker Red fluorescence or Nile blue sulphate vital 
      staining, displayed excessive apoptosis in the rostral hindbrain, specifically 
      within rhombomeres 1-3, as well as in cranial neural crest cells and ectodermal 
      placodes. Comparably treated embryos examined on GD 10.5-11 illustrated a 
      disproportionate reduction in the length of the rostral hindbrain. Examination of 
      plastic histological sections of GD 9 embryos and via scanning electron 
      microscopy on GD 10 revealed deficiencies in the hindbrain, with a phenotype 
      including abnormal rhombomere segmentation and an extremely small fourth 
      ventricular roofplate. Whole-mount antineurofilament immunohistochemistry on GD 
      10.5 and GD 11 illustrated a variety of cranial nerve abnormalities ranging from 
      fused or absent ganglia to ectopic or disorganized fibers. In addition, a delay 
      in the development of the glossopharyngeal (IX) nerve/ganglia complex was 
      observed. These hindbrain and cranial nerve abnormalities are discussed in the 
      context of the genesis of human alcohol-related birth defects and 
      neurodevelopmental disorder.
CI  - Copyright 2002 S. Karger AG, Basel
FAU - Dunty, William C Jr
AU  - Dunty WC Jr
AD  - Department of Cell and Developmental Biology and the Bowles Center for Alcohol 
      Studies, University of North Carolina at Chapel Hill, NC 27599-7090, USA.
FAU - Zucker, Robert M
AU  - Zucker RM
FAU - Sulik, Kathleen K
AU  - Sulik KK
LA  - eng
GR  - AA11605/AA/NIAAA NIH HHS/United States
GR  - DA-07244/DA/NIDA NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Switzerland
TA  - Dev Neurosci
JT  - Developmental neuroscience
JID - 7809375
RN  - 0 (Neurofilament Proteins)
RN  - 3K9958V90M (Ethanol)
SB  - IM
MH  - Alcohol-Induced Disorders, Nervous System/*pathology
MH  - Animals
MH  - Apoptosis
MH  - Cranial Nerves/abnormalities/*drug effects/metabolism/pathology
MH  - Ethanol/*toxicity
MH  - Female
MH  - Fetal Alcohol Spectrum Disorders/metabolism/*pathology
MH  - Immunohistochemistry
MH  - Injections, Intraperitoneal
MH  - Mice
MH  - Microscopy, Confocal
MH  - Microscopy, Electron, Scanning
MH  - Neurofilament Proteins/metabolism
MH  - Pregnancy
MH  - *Prenatal Exposure Delayed Effects
MH  - Rhombencephalon/abnormalities/*drug effects/pathology/ultrastructure
MH  - Time Factors
EDAT- 2002/11/29 04:00
MHDA- 2003/03/18 04:00
CRDT- 2002/11/29 04:00
PHST- 2002/11/29 04:00 [pubmed]
PHST- 2003/03/18 04:00 [medline]
PHST- 2002/11/29 04:00 [entrez]
AID - 66748 [pii]
AID - 10.1159/000066748 [doi]
PST - ppublish
SO  - Dev Neurosci. 2002;24(4):328-42. doi: 10.1159/000066748.