PMID- 12774854
OWN - NLM
STAT- MEDLINE
DCOM- 20040123
LR  - 20131121
IS  - 0008-4212 (Print)
IS  - 0008-4212 (Linking)
VI  - 81
IP  - 5
DP  - 2003 May
TI  - Chronic prenatal ethanol exposure-induced decrease of guinea pig hippocampal CA1 
      pyramidal cell and cerebellar Purkinje cell density.
PG  - 476-84
AB  - The brain is a key target of ethanol teratogenicity, in which ethanol can produce 
      neurodegeneration in selected areas, including the hippocampus and cerebellum. 
      The research objective was to test the hypothesis that chronic prenatal ethanol 
      exposure, via maternal ethanol administration, produces differential time course 
      of decreased linear density of hippocampal CA1 pyramidal cells and cerebellar 
      Purkinje cells. Timed pregnant guinea pigs received chronic oral administration 
      of ethanol, isocaloric-sucrose/pair-feeding, or water throughout gestation (term, 
      about gestational day (GD) 68), and the offspring were studied at GD 62 
      (near-term fetus), postnatal day (PD) 1 (neonate), PD 5, and PD 12 (early 
      postnatal life). Ethanol treatment, compared with isocaloric-sucrose/pair-feeding 
      and water treatments, decreased brain, hippocampal, and cerebellar weights at GD 
      62, PD 1, PD 5, and PD 12. Hippocampal CA1 pyramidal cell linear density and 
      cerebellar Purkinje cell linear density were unaffected at GD 62. Ethanol 
      treatment produced 25, 30, and 30% decreases in linear density of hippocampal CA1 
      pyramidal cells at PD 1, PD 5, and PD 12, respectively, and a 30% decrease in 
      linear density of cerebellar Purkinje cells at PD 12 only. At PD 5, Purkinje cell 
      profile linear density remained unaffected; however, ethanol treatment appeared 
      to increase linear density of apoptotic Purkinje cell nuclei, as determined by a 
      modified TUNEL method. The data demonstrate that chronic prenatal ethanol 
      exposure produces apparent differential time course of decreased linear density 
      of hippocampal CA1 pyramidal cells and cerebellar Purkinje cells in the 
      developing guinea pig.
FAU - McGoey, Tara N
AU  - McGoey TN
AD  - Department of Pharmacology & Toxicology, Faculty of Health Sciences, Queen's 
      University, Kingston, ON K7L 3N6, Canada.
FAU - Reynolds, James N
AU  - Reynolds JN
FAU - Brien, James F
AU  - Brien JF
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Canada
TA  - Can J Physiol Pharmacol
JT  - Canadian journal of physiology and pharmacology
JID - 0372712
RN  - 0 (Teratogens)
RN  - 3K9958V90M (Ethanol)
SB  - IM
MH  - Administration, Oral
MH  - Animals
MH  - Animals, Newborn
MH  - Apoptosis/drug effects
MH  - Cell Count
MH  - Cerebellum/cytology/drug effects
MH  - Dentate Gyrus/cytology/drug effects/growth & development
MH  - Ethanol/*toxicity
MH  - Female
MH  - Guinea Pigs
MH  - Hippocampus/cytology/*embryology/growth & development
MH  - In Situ Nick-End Labeling
MH  - Organ Size/drug effects
MH  - Pregnancy
MH  - *Prenatal Exposure Delayed Effects
MH  - Purkinje Cells/cytology/*drug effects
MH  - Pyramidal Cells/cytology/*drug effects
MH  - Teratogens/*toxicity
EDAT- 2003/05/31 05:00
MHDA- 2004/01/24 05:00
CRDT- 2003/05/31 05:00
PHST- 2003/05/31 05:00 [pubmed]
PHST- 2004/01/24 05:00 [medline]
PHST- 2003/05/31 05:00 [entrez]
AID - y03-048 [pii]
AID - 10.1139/y03-048 [doi]
PST - ppublish
SO  - Can J Physiol Pharmacol. 2003 May;81(5):476-84. doi: 10.1139/y03-048.