PMID- 16528705
OWN - NLM
STAT- MEDLINE
DCOM- 20060609
LR  - 20131121
IS  - 1542-9733 (Print)
IS  - 1542-9733 (Linking)
VI  - 77
IP  - 2
DP  - 2006 Apr
TI  - Failure of homocysteine to induce neural tube defects in a mouse model.
PG  - 89-94
AB  - BACKGROUND: Folate deficiencies have been associated with many adverse congenital 
      abnormalities. It is not clear, however, whether these defects are due to a 
      folate deficiency or to an increase in homocysteine. Homocysteine has been shown 
      to be teratogenic in the chicken-embryo model and it has been suggested that 
      homocysteine-induced defects are mediated by inhibiting the N-methyl-D-aspartate 
      (NMDA) receptor on neural crest cells. The majority of the teratology studies 
      have been carried out using the chicken embryo model. In an effort to develop a 
      murine model of homocysteine-induced neural tube defects, several inbred mouse 
      strains were treated with homocysteine or the NMDA inhibitor MK801 and the 
      fetuses examined for any induced-NTD. METHODS: Several in-bred mouse strains were 
      administered homocysteine once on gestational day (GD) E8.5 or once daily on GD 
      6.5-10.5. Additionally, because homocysteine was been reported to mediate its 
      effects through the NMDA receptor, the effect of MK801, an antagonist of this 
      receptor, was also investigated. RESULTS: Regardless of the mouse treatment time, 
      homocysteine failed to induce neural tube defects in our in-bred mouse strains. 
      Homocysteine also failed to increase the number of neural tube defects in the 
      splotch strain, regardless of the genotype. CONCLUSIONS: Irrespective of the 
      mouse strain or treatment, homocysteine failed to induce neural tube defects in 
      our mouse models, which is in contrast to what has been reported in the chicken 
      embryo models.
CI  - Birth Defects Res (Part B) 77:89-94, 2006. (c) 2006 Wiley-Liss, Inc.
FAU - Bennett, Gregory D
AU  - Bennett GD
AD  - Department of Genetics Cell Biology and Anatomy, University of Nebraska Medical 
      Center, Omaha, Nebraska 68198-5805, USA. gbennett@unmc.edu
FAU - Vanwaes, Janee
AU  - Vanwaes J
FAU - Moser, Kristine
AU  - Moser K
FAU - Chaudoin, Tammy
AU  - Chaudoin T
FAU - Starr, Lois
AU  - Starr L
FAU - Rosenquist, Thomas H
AU  - Rosenquist TH
LA  - eng
GR  - P01-HL66398/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Birth Defects Res B Dev Reprod Toxicol
JT  - Birth defects research. Part B, Developmental and reproductive toxicology
JID - 101155115
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 462-10-2 (Homocystine)
RN  - 6LR8C1B66Q (Dizocilpine Maleate)
SB  - IM
MH  - Animals
MH  - *Disease Models, Animal
MH  - Dizocilpine Maleate/pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Homocystine/*toxicity
MH  - Mice/*abnormalities
MH  - Mice, Inbred Strains
MH  - Neural Tube Defects/*chemically induced
MH  - Receptors, N-Methyl-D-Aspartate/*antagonists & inhibitors
EDAT- 2006/03/11 09:00
MHDA- 2006/06/10 09:00
CRDT- 2006/03/11 09:00
PHST- 2006/03/11 09:00 [pubmed]
PHST- 2006/06/10 09:00 [medline]
PHST- 2006/03/11 09:00 [entrez]
AID - 10.1002/bdrb.20071 [doi]
PST - ppublish
SO  - Birth Defects Res B Dev Reprod Toxicol. 2006 Apr;77(2):89-94. doi: 
      10.1002/bdrb.20071.