Objective: To study the role of N-methyl-D-aspartate receptor 1 in acute intoxicated encephalopathy induced by 1,2- dichloroethane(1,2-DCE).
Methods: Forty-two Sprague-Dawley rats, which had been randomly divided into 1 control, 3 exposure and 3 after-exposure observation groups were exposed to 1,2-DCE for 12 hr by continual static inhalation except control group. Dosage of exposure groups was 5.0, 10.0, 20.0 g/m(3) on sequence. That of after-exposure observation groups was 10.0 g/m(3). Rats of after-exposure observation groups were observed continually for 2,4,6 hr after exposure. The expression of N-methyl-D-aspartate receptor-1 (NMDAR1) was detected by immunohistochemical method.
Results: NMDAR1 stained neurons were mainly distributed at cerebral cortex and hippocampus. Compared with that of control group, the percentages of positive cells of NMDAR1 increased evidently at 10.0, 20.0 g/m(3) groups (P < 0.05). They were (18.33 +/- 1.86)%, (64.17 +/- 2.86)% at cerebral cortex, (15.5 +/- 1.87)%, (47.83 +/- 2.16)% at hippocampus. The percentages were also elevated obviously in 2, 4, 6 h after-exposure observation groups. They were (39.07 +/- 3.01)% (70.17 +/- 2.93)% (39.83 +/- 2.32)% at cerebral cortex, (16.30 +/- 1.03)% (19.80 +/- 1.17)% (16.50 +/- 1.05)% at hippocampus; Compared with that of 10.0 g/m(3) group, the percentages increased significantly only in 4 hr group at hippocampus.
Conclusion: The overactivation of NMDAR1 is the main route by which excitatory amino acids chose to join the development of acute intoxicated encephalopathy induced by 1,2-DCE.