Mechanisms underlying the antimotion sickness effects of psychostimulants.

The major conclusions of this review are: 1) that selective enhancement of dopaminergic transmission, not noradrenergic, is sufficient to account for amphetamine-induced resistance and perhaps natural resistance to motion sickness; 2) the site of this enhanced dopaminergic transmission is probably within the basal ganglia; and 3) the neuropharmacology of the basal ganglia, but not the brainstem vestibular areas, can account for the therapeutic synergism of scopolamine and amphetamine. The therapeutic actions of psychostimulants may be dissociable from some of their side effects, particularly cardiovascular effects related to peripheral norepinephrine release. Drugs which target specific subtypes of dopaminergic receptors may serve this purpose.