Alpha-noradrenaline modulation of D,L-allylgycine seizures.
The preferential alpha 2-noradrenergic agonist clonidine dose-relatedly increased the onset of seizures and mortality times, and decreased severity in rats treated with D,L-allylglycine. These effects were reduced by a dose (2.5 mg/kg) of the preferential alpha 2-antagonist yohimbine, which was itself inactive on the allylglycine seizures. Yohimbine 10 mg/kg alone decreased onset and mortality times. The preferential alpha 1-antagonist prazosin had a slight anticonvulsant effect. These results suggest that the reduction of NA release at alpha 2-noradrenergic receptors or antagonism of noradrenaline effects at alpha 1-receptors exerts seizure suppressant effects.
D000501:Allylglycine / Q000633:toxicity*; D000818:Animals; D003000:Clonidine / Q000494:pharmacology; D005998:Glycine / Q000031:analogs & derivatives*; D008297:Male; D009638:Norepinephrine / Q000378:metabolism*; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011941:Receptors, Adrenergic / Q000187:drug effects*; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects*; D012640:Seizures / Q000139:chemically induced*; D015016:Yohimbine / Q000494:pharmacology
D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D000501:Allylglycine; D015016:Yohimbine; D003000:Clonidine; D005998:Glycine; D009638:Norepinephrine; D011224:Prazosin