PMID- 10231169
OWN - NLM
STAT- MEDLINE
DCOM- 19990625
LR  - 20190915
IS  - 0741-8329 (Print)
IS  - 0741-8329 (Linking)
VI  - 17
IP  - 3
DP  - 1999 Apr
TI  - Chronic ethanol exposure alters MK-801 binding sites in the cerebral cortex of 
      the near-term fetal guinea pig.
PG  - 215-21
AB  - The mechanism of ethanol central nervous system (CNS) teratogenesis, resulting 
      from chronic maternal ingestion of high-dose ethanol during pregnancy, is not 
      clearly understood. One of the target sites for ethanol-induced damage in the 
      developing brain is the cerebral cortex. It has been proposed that chronic 
      prenatal ethanol exposure alters NMDA receptors in the developing cerebral 
      cortex. To test this hypothesis, timed pregnant guinea pigs were administered one 
      of the following oral treatments throughout gestation: 4 g ethanol/kg maternal 
      body weight/day; isocaloric sucrose/pair-feeding; water; or no treatment (ad 
      lib). Near-term fetuses were studied at gestational day (GD) 63 (term, about GD 
      68). This ethanol regimen produced a maternal blood ethanol concentration of 
      66+/-4 mM (304+/-19 mg/dl) at 1 h after the daily dose on GD 58. The chronic 
      ethanol regimen decreased near-term fetal body weight (12-26% decrease), brain 
      weight (23% decrease), and cerebral cortical weight (21% decrease), compared with 
      the isocaloric sucrose/pair-feeding, and combined water/ad lib experimental 
      groups. Saturation analysis of near-term fetal cerebral cortical membranes using 
      a [3H]MK-801 radioligand binding assay demonstrated a decreased affinity and 
      increased number of MK-801 binding sites for the chronic ethanol regimen compared 
      with the control treatments. These data support the suggestion that upregulation 
      of NMDA receptors in the cerebral cortex after chronic prenatal ethanol exposure 
      could lead to NMDA receptor-mediated excitotoxicity in this brain region.
FAU - Chiu, J
AU  - Chiu J
AD  - Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario, 
      Canada.
FAU - Brien, J F
AU  - Brien JF
FAU - Wu, P
AU  - Wu P
FAU - Eubanks, J H
AU  - Eubanks JH
FAU - Zhang, L
AU  - Zhang L
FAU - Reynolds, J N
AU  - Reynolds JN
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Alcohol
JT  - Alcohol (Fayetteville, N.Y.)
JID - 8502311
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 3K9958V90M (Ethanol)
RN  - 6LR8C1B66Q (Dizocilpine Maleate)
SB  - IM
MH  - Animals
MH  - Body Weight/drug effects
MH  - Brain/drug effects/embryology
MH  - Cerebral Cortex/*embryology/*metabolism
MH  - Dizocilpine Maleate/*metabolism
MH  - Ethanol/*administration & dosage/blood
MH  - Female
MH  - Fetal Blood/chemistry
MH  - Fetus/drug effects
MH  - Gestational Age
MH  - Guinea Pigs
MH  - Maternal-Fetal Exchange
MH  - Organ Size/drug effects
MH  - Pregnancy
MH  - Receptors, N-Methyl-D-Aspartate/*drug effects/metabolism
EDAT- 1999/05/07 00:00
MHDA- 1999/05/07 00:01
CRDT- 1999/05/07 00:00
PHST- 1999/05/07 00:00 [pubmed]
PHST- 1999/05/07 00:01 [medline]
PHST- 1999/05/07 00:00 [entrez]
AID - S0741-8329(98)00050-0 [pii]
AID - 10.1016/s0741-8329(98)00050-0 [doi]
PST - ppublish
SO  - Alcohol. 1999 Apr;17(3):215-21. doi: 10.1016/s0741-8329(98)00050-0.