A nitric oxide (NO) synthase inhibitor accelerates amygdala kindling.
In response to NMDA receptor activation, hippocampal, striatal and cerebellar neurons synthesize nitric oxide (NO), which in turn elevates cGMP levels via guanylate cyclase. NO is increasingly being considered as a transsynaptic retrograde messenger, involved in neuronal plasticity. The effect of an inhibitor of NO synthase, L-NG-nitroarginine (NOArg), was studied on amygdala kindling and on kindled seizures in rats. NOArg increased kindling rate, particularly in its initial period, but did not modify seizure severity in previously kindled rats, although we have no definitive explanation for this effect. However, an enhanced post-synaptic excitability could be attributed to the blockade of the negative feed-back exerted by NO on the NMDA receptor.
Rondouin
G
G
Laboratoire de Médecine Expérimentale, CNRS UPR9008, INSERM U249, Montpellier, France.
Lerner-Natoli
M
M
Manzoni
O
O
Lafon-Cazal
M
M
Bockaert
J
J
D000594:Amino Acid Oxidoreductases / Q000037:antagonists & inhibitors*; D000679:Amygdala / Q000187:drug effects*; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000494:pharmacology; D006152:Cyclic GMP / Q000378:metabolism; D004827:Epilepsy / Q000139:chemically induced*; D007696:Kindling, Neurologic / Q000187:drug effects*; D008297:Male; D009473:Neuronal Plasticity / Q000187:drug effects*; D019001:Nitric Oxide Synthase; D019335:Nitroarginine; D051381:Rats; D017207:Rats, Sprague-Dawley
D019335:Nitroarginine; D001120:Arginine; D019001:Nitric Oxide Synthase; D000594:Amino Acid Oxidoreductases; D006152:Cyclic GMP