Nitric Oxide–Mediated Modification of the Glycine Binding Site of the NMDA Receptor During Hypoxia in the Cerebral Cortex of the Newborn Piglet
Autor: | Om P. Mishra, Nehal A. Parikh, Syed Hassan Haider, Maria Delivoria Papadopoulos, David F. Sorrentino, Karen I. Fritz |
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Rok vydání: | 2004 |
Předmět: |
medicine.medical_specialty
Indazoles Swine Glycine Nitric Oxide Receptors N-Methyl-D-Aspartate Biochemistry Nitric oxide Cellular and Molecular Neuroscience chemistry.chemical_compound Glycine binding Internal medicine medicine Animals Enzyme Inhibitors Hypoxia Receptor Cerebral Cortex Binding Sites Cerebral hypoxia General Medicine Hypoxia (medical) medicine.disease medicine.anatomical_structure Endocrinology Animals Newborn chemistry Cerebral cortex Apoptosis NMDA receptor Nitric Oxide Synthase medicine.symptom |
Zdroj: | Neurochemical Research. 29:455-459 |
ISSN: | 0364-3190 |
DOI: | 10.1023/b:nere.0000013751.17464.ee |
Popis: | This study tested the hypothesis that cerebral hypoxia results in nitric oxide (NO)-mediated modification of the glycine-binding site of the N-methyl-D-aspartate (NMDA) receptor. Glycine binding characteristics were determined in normoxic, hypoxic, and hypoxic with 7-nitroindazole (7-NINA)-pretreated newborn piglets. The role of nitration was evaluated by determining binding characteristics in non-nitrated and in-vitro nitrated membranes. Bmax and Kd values were 30% higher in the hypoxic group than the normoxic and 7-NINA pretreated hypoxic groups. Kd values in the in-vitro normoxic nitrated membranes were similar to the non-nitrated hypoxic group. Bmax values in the in-vitro) normoxic nitrated membrane samples were 16% lower than in the non-nitrated hypoxic group. We conclude cerebral hypoxia causes modification of the glycine-binding site of the NMDA receptor and this modification of the glycine-binding site may be NO mediated. We propose that NO-mediated modification of the glycine-binding site of the NMDA receptor regulates calcium influx through its ion-channel. |
Databáze: | OpenAIRE |
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