Central Nervous System and Autonomic Nervous System Effects of Amantadine and of Some Standard Anti-Parkinson Drugs

Abstract

The activity of amantadine HCl, trihexyphenidyl HCl, ethopropazine HCl, atropine sulphate, mecamylamine HCl and L-dopa against effects provoked by nicotine injected intracerebrally(tremors, convulsions, loss of righting reflex) was studied. The antagonistic drugs were injected intraperitoneally or intracerebrally.The above mentioned drugs except L-dopa and atropine preventednicotine manifestations when given intraperitoneally. Amantadine, atropine and mecamylamine, resulted active when given intracerebrally (trihexyphenidyl, ethopropazine and L-dopa could not betested i.e.). Effects provoked by oxotremorine were counteracteby atropine, trihexyphenidyl, ethopropazine but not by amantadineand mecamylamine. Trihexyphenidyl, ethopropazine and atropine had anticarbamylcholine activity and mydriatic activity. Amantadine and mecamylamine were inactive or almost inactive.

Responses of Neurones in the Cerebral Cortex and Caudate Nucleus to Amantadine, Amphetamine and Dopamine

“…Although cholinergic nerve endings are present in the cortex and striatum, amantadine's effects are not likely to be due to an effect on such terminals, since amantadine has been shown to have very little effect on peripheral cholinergic systems (Vernier, Harmon, tump, Lynes, Marvel & Smith, 1969;Grelak et al, 1970;Bianchi & Tomasi, 1973). The primarily depressant action of dopamine on striatal neurones is consistent with the idea that most nigrostriatal dopaminergic neurones are inhibitory to caudate cells (McLennan & York, 1967;Connor, 1970).…”