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The antiparkinsonian drug amantadine HCl caused a dose-dependent depression of electrical self-stimulation, followed by a dose-dependent enhancement. Neither action was correlated with the differential effects of d- and l-amphetamine at different implantation sites. The initial depression was not prevented by pretreatment with anticholinergic or antiserotonergic agents nor by depression of catecholamine (CA) synthesis. The stimulant effects of amantadine and d-amphetamine summated but did not interact, response rates after d-amphetamine being augmented by pretreatment with amantadine except at intervals at which amantadine was by itself depressant. It is concluded that the initial effect of amantadien is caused by impulse-independent release of a pool of intraneuronal CA, causing dissociation between reinforcement signals and the rat's responses. This is followed by amphetamine-like facilitation of impulse-dependent release; the first action depresses performance, the second enhances it.
L J Herberg, and
D N Stephens
March 1977,
Psychopharmacology,
L J Herberg, and
D N Stephens
January 1977,
Experientia,
L J Herberg, and
D N Stephens
February 1976,
Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.),
L J Herberg, and
D N Stephens
November 1969,
Archives internationales de pharmacodynamie et de therapie,
L J Herberg, and
D N Stephens
January 1964,
Federation proceedings,
L J Herberg, and
D N Stephens
June 1975,
British journal of pharmacology,
L J Herberg, and
D N Stephens
June 1972,
Archives internationales de pharmacodynamie et de therapie,
L J Herberg, and
D N Stephens
January 1967,
Psychopharmacologia,
L J Herberg, and
D N Stephens
January 1966,
Psychopharmacologia,
L J Herberg, and
D N Stephens
October 1973,
Neuropharmacology,
