Buisson A, Lakhmeche N, Verrecchia C, Plotkine M, Boulu R G
Laboratoire de Pharmacologie, Faculté des Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France.
Neuroreport. 1993 Apr;4(4):444-6.
In the present study, we examine the involvement of the L-arginine-nitric oxide pathway in seizure activity termination. Convulsions were induced reproducibly by intracerebroventricular administration of N-methyl-D-aspartate to conscious mice. The duration of the seizure activity was increased by inhibition of the NO-pathway or by intracerebroventricular injection of methylene blue, an inhibitor of guanylate cyclase activity. This increased duration in seizure activity was reversed by co-administration of L-arginine or by intracerebroventricular injection of guanosine 3':5' cyclic monophosphate (cGMP). These results suggest that nitric oxide produced in response to NMDA receptor activation leads to an increase in cGMP which induces the seizure activity termination.
