Peroxynitrite-induced modification of the N-methyl-D-aspartate receptor in the cerebral cortex of the guinea pig fetus at term
SA Zanelli, QM Ashraf, M Delivoria-Papadopoulos… - Neuroscience …, 2000 - Elsevier
SA Zanelli, QM Ashraf, M Delivoria-Papadopoulos, OP Mishra
Neuroscience letters, 2000•ElsevierThe present study tests the hypothesis that nitration is a potential mechanism of N-methyl-d-
aspartate (NMDA) receptor modification, by assessing the effect of peroxynitrite in vitro on
the glutamate and ion-channel sites of the NMDA receptor in the fetal guinea pig. Nitration of
NMDA receptor subunits was confirmed by Western blot. Following peroxynitrite exposure,
3H-MK-801 bindings show an increase in the Bmax and a decrease in the Kd, while 3H-
glutamate bindings show a decrease in the Kd with no change in the Bmax. We conclude …
aspartate (NMDA) receptor modification, by assessing the effect of peroxynitrite in vitro on
the glutamate and ion-channel sites of the NMDA receptor in the fetal guinea pig. Nitration of
NMDA receptor subunits was confirmed by Western blot. Following peroxynitrite exposure,
3H-MK-801 bindings show an increase in the Bmax and a decrease in the Kd, while 3H-
glutamate bindings show a decrease in the Kd with no change in the Bmax. We conclude …
The present study tests the hypothesis that nitration is a potential mechanism of N-methyl-d-aspartate (NMDA) receptor modification, by assessing the effect of peroxynitrite in vitro on the glutamate and ion-channel sites of the NMDA receptor in the fetal guinea pig. Nitration of NMDA receptor subunits was confirmed by Western blot. Following peroxynitrite exposure, 3H-MK-801 bindings show an increase in the Bmax and a decrease in the Kd, while 3H-glutamate bindings show a decrease in the Kd with no change in the Bmax. We conclude that peroxynitrite regulates the NMDA receptor function by increasing the affinity of the ion-channel and glutamate sites, and by exposing additional ion-channel sites. We propose that nitration of the NMDA receptor is a potential mechanism for the regulation of the receptor during hypoxia.
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