Enhancement of N-methyl-D-aspartateNMDA Receptor 2B-mediated Neurotoxi-city after Hypoxia in the Rat Hippocampal Formation.
- Author:
Yong Wook JUNG
;
So Hee HAM
;
Il Soo MOON
;
Bok Hyun KO
- Publication Type:Original Article
- Keywords:
Hypoxia;
NR2B;
MAP2;
NF200
- MeSH:
Animals;
Anoxia*;
Brain;
Cell Death;
Cell Membrane;
Cytoskeleton;
Eosinophils;
Hippocampus*;
N-Methylaspartate;
Neurons;
Peptide Hydrolases;
Proteolysis;
Rats*;
Receptors, N-Methyl-D-Aspartate;
Tolonium Chloride
- From:Korean Journal of Anatomy
1997;30(4):361-374
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Ischemic brain hippocampal formation has been developed to understand the relationship between delayed neuronal damage and the expression of NMDA receptor subunits[NR2A, NR2B], MAP2, and NF200 in ttle conditions of hypoxia. Changes of NR subunits[NR2A, 2B], MAP2 6nd NF200 in rat brain postsynaptic density[PSD] after hypoxic injury were investigated through immunoblot analyses. To understand the effect of Ca2+ influx through NMDA receptors on neuronal damage which is manifested by morphological change, cytoskeletal disruption was examined through H & E, toluidine blue and immunohistochemical studies. The expression of NR2B was increased than normal at 30 hours after hypoxia. At this time, the expression of MAP2 and NF200 was markedly decreased and their morphology was more eosinophilic than normal and then became darker with expanded perineuronal space. Irreversible neuronal cell damage in hypoxic hippocampal formation is most prominent in CA3 region of hippocampus and the process is triggered by Ca2+ influx through NR1/MR2B receptor channel at 30 hour after initial hypoxic insult. Ca2+ influx through NR1/MR2B receptor channel may activate intracellular proteases which would degrade cytoskeleton. Proteolysis of cytoskeleton leads to its reorganization and eventually damages normal function of cell membrane which causes neuronal cell death. And, morphological changes of neuronal cells in hypoxic conditions were manifested as red neurons in the stage of reactive change, and as dark neuron in the stage of late hypoxic cell damage.
