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| Expression and significance of hippocampal NMDA receptor subunit NR2B after traumatic brain injury in mice |
| Wang Wei, Wang Qian-mei, Yin Wen |
| Department of Emergency, Xijing Hospital, Air Force Military Medical University, Xi′an 710032, China |
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Abstract Objective To explore the expression pattern and significance of N-methyl-D-aspartic acid (NMDA) receptor subunit NR2B in hippocampal after traumatic brain injury (TBI). Methods Seventy-two Balb/c mice were randomly divided into sham group, TBI group and Ifenprodil treated group (TBI+IF group). TBI model was established by a control cortical injury device; mice in TBI+IF group were injected with Ifenprodil intraperitoneally for 1 week post injury. Western-blotting was used to detect the expression of hippocampal NR2B and phosphorylated NR2B (pNR2B). Morris water maze (MWM) test was used to study learning and memory capacity of mice. Results Compared to sham group (0.47±0.03 and 0.39±0.04), hippocampal NR2B and pNR2B levels increased in TBI group at 1 day post injury (3.54±0.15 and 3.27±0.36), and reduced gradually from 1 d, 3 d to 7 d, but the level at 3 day and 7 day post injury(1.21±0.11 and 1.28±0.07) was still higher than that of sham group(P<0.05). NR2B and pNR2B expression were significantly decreased in TBI+IF group than those in TBI group at the three time points. MWM tests found that escape latency was increased in TBI group (29.39±4.67)s compared to sham group (17.55±2.90)s, platform crossing times and target quadrant duration were decreased in TBI group (2.97±0.63 and 19.57±4.08)s compared to sham group 12.01±3.65 vs. (48.67±6.13)s. In comparison with TBI group, escape latency (15.89±2.90)s was evidently reduced, platform crossing times and target quadrant duration 10.41±2.54 and (51.82±9.26)s were increased in TBI+IF group. Conclusion Hippocampal NR2B and pNR2B expression are significantly increased after TBI, inhibition of NR2B and pNR2B can rescue the cognitive dysfunction caused by TBI.
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Corresponding Authors:
Yin Wen, E-mail: xjyyyw@126.com
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