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N‐methyl‐D‐aspartate receptors: Transient loss of NR1/NR2A/NR2B subunits after traumatic brain injury in a rodent model
Author(s) -
Kumar Arvind,
Zou Linglong,
Yuan Xiaoqing,
Long Yan,
Yang Keyi
Publication year - 2002
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.10181
Subject(s) - nmda receptor , traumatic brain injury , hippocampus , hippocampal formation , western blot , protein subunit , receptor , medicine , neuroscience , endocrinology , messenger rna , pathophysiology , biology , chemistry , anesthesia , biochemistry , gene , psychiatry
Hippocampal N‐methyl‐D‐aspartate (NMDA) receptor subunits, by virtue of their involvement in excitotoxic injury as well as memory association, may play an important role in the pathophysiologic mechanisms of traumatic brain injury (TBI). In this study, temporal changes in NMDA receptor subunit (NR1, NR2A, and NR2B) levels in rat hippocampus after TBI were investigated by Western blot and mRNA expression levels by RT‐PCR methods. Sprague‐Dawley rats (250–350 g) were employed, and a controlled cortical impact injury device was used to produce the TBI in rodents. At different postinjury time points (2, 6, 12, 24, and 48 hr), the rat hippocampi were dissected out for protein and RNA preparation. Western blot analysis revealed significant decreases of NR1, NR2A, and NR2B subunit proteins at 6 and 12 hr postinjury in rat hippocampus. Complete recovery of NR1, NR2A, and NR2B subunit protein to the levels of sham controls was observed at 24 hr postinjury. However, RT‐PCR analysis did not show any significant change in the mRNA levels at 2, 6, and 12 hr postinjury in comparison with sham controls, suggesting nontranscriptional change in the levels of these subunits. Thus, TBI can produce transient degradation of NMDA receptor subunits in the hippocampus, which might contribute to temporary memory impairment after injury. © 2002 Wiley‐Liss, Inc.