Further Studies on the Mode of Action of Amantadine

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Abstract
The anti‐Parkinson agent amantadine, when administered to rats and mice, was found to cause increased motor activity in mice, and an increased flexor reflex activity in acutely spinalized rats and rotation to the side of the lesion in unilaterally striatotomized rats. This last‐mentioned effect was inhibited by blockers of the dopamine (DA) receptors in the corpus striatum and by previous depletion of the catecholamines (CA). The drug was found to reduce NA accumulation after L‐DOPA administration to mice pretreated with reserpine and nialamide while the endogenous CA‐levels remained almost unaffected. The CA‐depletion seen after the administration of H 77/77 (4,α‐dimethyl‐metatyramine) was only slightly prevented, indicating that amantadine only to a small extent inhibits the uptake mechanism at the level of the cell membrane. Moreover, studies on brain homogenates revealed, that amantadine probably does not inhibit monoamine oxidase. It is concluded that the anti‐Parkinson effect of amantadine might well be explained by a release of CA in the brain – i.e. particularly of DA in the neostriatum.

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