PMID- 11754172
OWN - NLM
STAT- MEDLINE
DCOM- 20020225
LR  - 20131121
IS  - 0040-3709 (Print)
IS  - 0040-3709 (Linking)
VI  - 64
IP  - 6
DP  - 2001 Dec
TI  - Increased cell death in the developing vestibulocochlear ganglion complex of the 
      mouse after prenatal ethanol exposure.
PG  - 301-10
AB  - BACKGROUND: Previous studies have demonstrated that excessive prenatal alcohol 
      exposure can damage the auditory and vestibular systems, in particular, cochlear 
      hair cells. However, the direct effect of ethanol on the peripheral neurons in 
      these pathways has not been examined. To study the effects of prenatal ethanol 
      exposure on the developing vestibulocochlear ganglion (VCG) complex and the 
      peripheral sensory organs, we exposed pregnant mice to ethanol and examined the 
      levels of cell death in the inner ear. METHODS: Pregnant C57BL/6J mice were 
      administered one of three doses of either ethanol (3.0, 4.5, and 5.5 g/kg) or 
      isocaloric maltose/dextrin via intragastric intubation on gestational day (GD) 
      12.5. Embryos were dissected out of the uterus 8 hr after the intubation. Dying 
      cells in the inner ear were stained with Nissl stain and labeled by in situ 
      terminal dUTP nick-end labeling (TUNEL), and the percentage of dying cells was 
      quantified. RESULTS: Ethanol exposure produced region-specific effects, with 
      ethanol-exposed embryos exhibiting enhanced cell death only in the VCG complex, 
      and not in the primitive saccule, cochlea, semicircular canal, or endolymphatic 
      sac. The effects of ethanol on cell death in the VCG are dose dependent, with a 
      significant increase in the level of cell death found only at the higher doses. 
      CONCLUSIONS: Ethanol has a selective cytotoxic dose-dependent effect on the VCG 
      at GD 12.5 suggesting that loss of VCG neurons may contribute to hearing and /or 
      vestibular abnormalities in FAS children. Furthermore, the presence of 
      TUNEL-positive cells and DNA laddering is consistent with the cells undergoing 
      apoptotic cell death.
CI  - Copyright 2001 Wiley-Liss, Inc.
FAU - Du, X
AU  - Du X
AD  - Department of Anatomy and Neurobiology, University of Tennessee Health Science 
      Center, Memphis, Tennessee 38163, USA.
FAU - Hamre, K M
AU  - Hamre KM
LA  - eng
GR  - AAA11113/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Teratology
JT  - Teratology
JID - 0153257
RN  - 0 (Central Nervous System Depressants)
RN  - 3K9958V90M (Ethanol)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Cell Death
MH  - Central Nervous System Depressants/*adverse effects
MH  - Dose-Response Relationship, Drug
MH  - Ear, Inner/*cytology/*drug effects/pathology
MH  - Ethanol/*adverse effects
MH  - Female
MH  - Ganglia/*metabolism
MH  - In Situ Nick-End Labeling
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neurons/drug effects
MH  - Pregnancy
MH  - Time Factors
MH  - Vestibulocochlear Nerve/*cytology/*drug effects/pathology
EDAT- 2001/12/26 10:00
MHDA- 2002/02/28 10:01
CRDT- 2001/12/26 10:00
PHST- 2001/12/26 10:00 [pubmed]
PHST- 2002/02/28 10:01 [medline]
PHST- 2001/12/26 10:00 [entrez]
AID - 10.1002/tera.1085 [pii]
AID - 10.1002/tera.1085 [doi]
PST - ppublish
SO  - Teratology. 2001 Dec;64(6):301-10. doi: 10.1002/tera.1085.