PMID- 12757827
OWN - NLM
STAT- MEDLINE
DCOM- 20030819
LR  - 20190922
IS  - 0892-0362 (Print)
IS  - 0892-0362 (Linking)
VI  - 25
IP  - 3
DP  - 2003 May-Jun
TI  - Brain growth spurt-prenatal ethanol exposure and the guinea pig hippocampal 
      glutamate signaling system.
PG  - 303-10
AB  - This study tested the hypothesis that prenatal ethanol exposure (PEE) during the 
      brain growth spurt (BGS) in the guinea pig suppresses the glutamate-NMDA 
      receptor-nitric oxide synthase (NOS) signaling system in the developing 
      hippocampus. Pregnant guinea pigs [term, about gestational day (GD) 68] received 
      daily oral administration of 2 g ethanol/kg maternal body weight/day on GD 43 
      and/or GD 44 and then 4 g ethanol/kg maternal body weight/day from GD 45 to GD 
      62, isocaloric-sucrose/pair-feeding or water. Offspring were studied at GD 63 
      (near-term fetus) and postnatal day (PD) 10 (young postnatal life). Maternal 
      blood ethanol concentration during ethanol treatment, pregnancy outcome 
      variables, no change in spontaneous locomotor activity, and decreased brain and 
      cerebral cortical weight data were reported previously [Neurotoxicol. Teratol. 23 
      (2001) 355]. This BGS-PEE regimen did not affect hippocampal stimulated glutamate 
      release in young postnatal offspring, NMDA receptors as assessed by [3H]MK-801 
      binding, or NOS activity in near-term fetal offspring. Furthermore, BGS-PEE did 
      not affect the number of hippocampal CA1 and CA3 pyramidal cells and dentate 
      gyrus granule cells in defined locations of these three regions in the 
      hippocampal formation. These findings are in contrast to the effects of chronic 
      prenatal exposure to this ethanol regimen throughout gestation, including 
      suppression of the hippocampal glutamate-NMDA receptor-NOS signaling system, 
      decreased number of hippocampal CA1 pyramidal cells, increased spontaneous 
      locomotor activity, and impaired performance in the Morris water maze.
FAU - Byrnes, Michelle L
AU  - Byrnes ML
AD  - Department of Pharmacology and Toxicology, Faculty of Health Sciences, Queen's 
      University, K7L 3N6, Kingston, ON, 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  - United States
TA  - Neurotoxicol Teratol
JT  - Neurotoxicology and teratology
JID - 8709538
RN  - 0 (Central Nervous System Depressants)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 3K9958V90M (Ethanol)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
SB  - IM
MH  - Animals
MH  - Body Weight/drug effects
MH  - Brain/drug effects/*embryology/growth & development
MH  - Central Nervous System Depressants/*toxicity
MH  - Ethanol/*toxicity
MH  - Female
MH  - Glutamic Acid/metabolism
MH  - Guinea Pigs
MH  - Hippocampus/*embryology/enzymology/growth & development/metabolism
MH  - Nitric Oxide Synthase/metabolism
MH  - Organ Size/drug effects
MH  - Pregnancy
MH  - *Prenatal Exposure Delayed Effects
MH  - Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors
MH  - Signal Transduction/*drug effects
EDAT- 2003/05/22 05:00
MHDA- 2003/08/20 05:00
CRDT- 2003/05/22 05:00
PHST- 2003/05/22 05:00 [pubmed]
PHST- 2003/08/20 05:00 [medline]
PHST- 2003/05/22 05:00 [entrez]
AID - S0892036202003549 [pii]
AID - 10.1016/s0892-0362(02)00354-9 [doi]
PST - ppublish
SO  - Neurotoxicol Teratol. 2003 May-Jun;25(3):303-10. doi: 
      10.1016/s0892-0362(02)00354-9.