PMID- 14604765
OWN - NLM
STAT- MEDLINE
DCOM- 20040219
LR  - 20190901
IS  - 0165-3806 (Print)
IS  - 0165-3806 (Linking)
VI  - 145
IP  - 2
DP  - 2003 Nov 12
TI  - Ethanol effects on neonatal rat cortex: comparative analyses of neurotrophic 
      factors, apoptosis-related proteins, and oxidative processes during vulnerable 
      and resistant periods.
PG  - 249-62
AB  - The developing central nervous system (CNS) is highly susceptible to ethanol, 
      with acute or chronic exposure producing an array of anomalies and cell loss. 
      Certain periods of vulnerability have been defined for various CNS regions, and 
      are often followed by periods of relative ethanol resistance. In the present 
      study, neonatal rats were acutely exposed to ethanol during a time when peak cell 
      death is found in developing cerebral cortex (postnatal day 7; P7), and during a 
      later neonatal period of ethanol resistance (P21). Comparisons at the two ages 
      were made of basal levels of neurotrophic factors (NTFs), and in addition, 
      ethanol-mediated changes in NTFs, apoptosis-related proteins, antioxidant 
      activities, and generation of reactive oxygen species (ROS) were quantified at 0, 
      2, and 12 h following termination of exposure. It was found that at P21, basal 
      levels of NTF nerve growth factor (NGF) and brain-derived neurotrophic factor 
      (BDNF) were considerably higher than at P7, possibly affording protection against 
      ethanol neurotoxicity at this age. Following ethanol treatment at P7, 
      approximately equal numbers of pro-apoptotic and pro-survival changes were 
      produced, although most of the pro-apoptotic alterations occurred rapidly 
      following termination of treatment, a critical period for initiation of 
      apoptosis. At P21, however, the large majority of ethanol-mediated changes were 
      adaptive, favoring survival. We speculate that the capacity of the older CNS to 
      upregulate a number of protective elements within the cellular milieu serves to 
      greatly mitigate ethanol neurotoxicity, while in younger animals, such 
      adjustments are minimal, thus enhancing ethanol vulnerability within this 
      developing region.
FAU - Heaton, Marieta Barrow
AU  - Heaton MB
AD  - Department of Neuroscience, McKnight Brain Institute, University of Florida 
      College of Medicine, Box 100244, Gainesville, FL 32610-0244, USA. 
      heaton@ufbi.ufl.edu
FAU - Paiva, Michael
AU  - Paiva M
FAU - Madorsky, Irina
AU  - Madorsky I
FAU - Shaw, Gerry
AU  - Shaw G
LA  - eng
GR  - AA09128/AA/NIAAA NIH HHS/United States
GR  - AA12151/AA/NIAAA NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Brain Res Dev Brain Res
JT  - Brain research. Developmental brain research
JID - 8908639
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Reactive Oxygen Species)
RN  - 3K9958V90M (Ethanol)
SB  - IM
MH  - Adaptation, Physiological/drug effects/physiology
MH  - Alcohol-Induced Disorders, Nervous System/*metabolism/pathology/physiopathology
MH  - Animals
MH  - Animals, Newborn
MH  - Apoptosis/*drug effects/physiology
MH  - Cell Death/drug effects/physiology
MH  - Cell Survival/drug effects/physiology
MH  - Drug Resistance/physiology
MH  - Ethanol/*toxicity
MH  - Female
MH  - Fetal Alcohol Spectrum Disorders/*metabolism/pathology/physiopathology
MH  - Genes, bcl-2/drug effects/genetics
MH  - Male
MH  - Nerve Growth Factors/*drug effects/metabolism
MH  - Neuroprotective Agents/metabolism
MH  - Oxidative Stress/*drug effects/physiology
MH  - Pregnancy
MH  - *Prenatal Exposure Delayed Effects
MH  - Rats
MH  - Rats, Long-Evans
MH  - Reactive Oxygen Species/metabolism
MH  - Up-Regulation/drug effects/physiology
EDAT- 2003/11/08 05:00
MHDA- 2004/02/20 05:00
CRDT- 2003/11/08 05:00
PHST- 2003/11/08 05:00 [pubmed]
PHST- 2004/02/20 05:00 [medline]
PHST- 2003/11/08 05:00 [entrez]
AID - S0165380603002414 [pii]
AID - 10.1016/j.devbrainres.2003.08.005 [doi]
PST - ppublish
SO  - Brain Res Dev Brain Res. 2003 Nov 12;145(2):249-62. doi: 
      10.1016/j.devbrainres.2003.08.005.