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Published on: May 29, 2013
The expression of the NR1-subunit of the NMDA receptor during mouse and early chicken development
Gregory D Bennett1, Kristine Moser, Tammy Chaudoin
1Department of Genetics Cell Biology and Anatomy, University of Nebraska Medical Center, 985805 UNMC, Omaha, NE 68198-5805, USA. gbennett@unmc.edu
Abstract:
It has been suggested that homocysteine-induced defects are mediated by the inhibition of the N-methyl-d-aspartate (NMDA) receptor on neural crest cells. However, the majority of this work has been performed using the chicken embryo model. In an effort to better understand the molecular events involved a murine model of homocysteine-induced defects was sought. However, it has been previously shown that homocysteine failed to induce congenital defects in several strains of mouse. Therefore, in an effort to better understand the difference in the susceptibility between these two species we investigated the ontogeny of the NMDA receptor in the mouse and chicken. To determine the expression of the NMDA receptor we performed Western blot analysis using an antibody to the NR1-subunit of the NMDA receptor in both the chicken and mouse embryos. Further, we used RT-PCR to determine the temporal expression of this subunit in the murine embryos from gestational day 8.5 to 18.5 to confirm our Western blot analysis. Results from these studies demonstrated that the expression of the NMDA receptor was expressed during the early stages of development in the chick embryo but neither the transcript nor the protein was detected in mouse embryos until later in development. These results demonstrate that during the stages of neurulation and/or early heart development the expression of the NR1-subunit of the NMDA receptor was not detected. The expression of this gene increased and was detectable by gestational days 14.5-15.5 and continued to increase in its expression until term. Therefore, these experiments suggest that homocysteine-induced defects may be mediated via the NMDA receptor.
Insights
Homocysteine may cause birth defects by inhibiting the N-methyl-D-aspartate (NMDA) receptor. Mouse embryos lack NMDA receptor expression during early development, unlike chicks, suggesting a species-specific susceptibility to homocysteine-induced defects.
Area of Science:
- Developmental biology
- Neuroscience
- Teratology
Background:
- Homocysteine-induced defects are hypothesized to involve N-methyl-D-aspartate (NMDA) receptor inhibition.
- Previous studies primarily used chicken embryos, with limited success in establishing murine models.
Purpose of the Study:
- Investigate the ontogeny of the NMDA receptor in mouse and chicken embryos.
- Understand species-specific differences in susceptibility to homocysteine-induced defects.
Main Methods:
- Western blot analysis for NR1-subunit protein expression in both species.
- RT-PCR for temporal NR1-subunit transcript expression in murine embryos (gestational days 8.5-18.5).
Main Results:
- NMDA receptor expression detected early in chick embryo development.
- Neither NR1-subunit transcript nor protein was detected in mouse embryos during early neurulation and heart development.
- NR1-subunit expression became detectable in mouse embryos around gestational days 14.5-15.5, increasing until term.
Conclusions:
- The delayed expression of the NMDA receptor's NR1-subunit in mice correlates with their lower susceptibility to homocysteine-induced defects.
- These findings suggest that the NMDA receptor plays a role in mediating homocysteine-induced developmental abnormalities.
