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Publication AbstractsInvolvement of nitric oxide and N-methyl-D-aspartate in acute hypoxic altitude convulsion in mice.Chen C-H, Chen AC-H, Liu H-JAviat Space Environ Med 1997; 68:296-9 AbstractBackground: Altitude convulsion is a rather specific form of experimental convulsion which is induced by acute exposure to a hypobaric hypoxic condition. Several neurotransmitters have been shown to be involved in the mechanisms of altitude convulsions. However, their roles and interaction were not clear. Hypothesis: The novel neurotransmitter nitric oxide (NO) may be involved in the mechanisms of altitude convulsion through its neuronal signaling roles in relation to the NMDA receptor. Methods: There were 177 mice intraperitoneally administrated (i.p.) with several drugs. The altitude convulsion threshold (ACT) was used as an index to evaluate the acute hypoxic tolerance. Results: NO synthesis precursor, L-arginine (20, 40, 200, 800 mg/kg), resulted in a dose-dependent decrease in the ACT in mice, while the NO synthase (NOS) inhibitor, NG-nitro-L-arginine-methyl ester (L-NAME, 1.25, 2.50, 5.00 mg/kg, i.p.) increased the ACT. Pretreatment with L-NAME (5.0 mg/kg) prior to L-arginine (200 mg/kg) administration prevented the effect of decreasing ACT caused by L-arginine. Similarly, N-methyl-D-aspartate (NMDA, 2.5, 10.0, 20.0 mg/kg, i.p.) yielded a decrease in the ACT in mice and this decrease in hypoxic tolerance caused by NMDA can be prevented by pretreatment with either NMDA receptor antagonist 2-amino-5-phosphovalerate (AP-5, 20.0 mg/kg, i.p.) or NOS inhibitor L-NAME (5.0 mg/kg, i.p.). Conclusions: These findings suggest an important signaling role for nitric oxide and NMDA in the development of altitude convulsion and further support the hypothesized relationship between NMDA-receptor mediated neurotoxicity and nitric oxide.
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