Transiently catecholaminergic cells in the fetal rat express mRNA for glutamate NMDAR1 receptor

The N-methyl-D-aspartate (NMDA) subtype of the glutamate receptor has been shown to be vital to the development of the central nervous system. The purpose of this study was to determine if the neural crost-derived precursors which migrate to the primitive gut contain mRNA encoding for the NMDA recep...

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Veröffentlicht in:Brain research 1996-04, Vol.718 (1-2), p.117-123
Hauptverfasser: BURNS, G. A, ULIBARRI, C, STEPHENS, K. E
Format: Artikel
Sprache:eng
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Zusammenfassung:The N-methyl-D-aspartate (NMDA) subtype of the glutamate receptor has been shown to be vital to the development of the central nervous system. The purpose of this study was to determine if the neural crost-derived precursors which migrate to the primitive gut contain mRNA encoding for the NMDA receptor. Many of these enteric precursors briefly elaborate tyrosine hydroxylase (TH) and have been termed transiently catecholaminergic (TC) cells. TH-like immunoreactivity (TH-ir) serves as a marker for them. Immunocytochemistry combined with NMDAR1 in situ hybridization revealed that TH-ir cells in Day 14 rat embryos do express mRNA coding for the NMDAR1 receptor. However, the TC cells did not contain detectable levels of immunoreactivity for the NMDAR1 receptor peptide. The absence of detectable NMDAR1-like immunoreactivity might reflect some form of transcriptional or translational regulation, such that the onset of functional receptor activity is delayed until differentiation and/or synaptogenesis commence. Whether TC cell migration is glutamate-mediated remains unclear, since some of them successfully reached the gut without expressing NMDAR1 message. Characterizing TC cell NMDA receptor activity and determining exactly when it ensues will be of paramount importance to defining the role(s) of this receptor in ENS development. In conclusion, the expression of NMDAR1 mRNA by TH-ir cells suggests a possible developmental role for this receptor.
ISSN:0006-8993
1872-6240
DOI:10.1016/0006-8993(96)00082-0