Abstract

In animals the pharmacological action of thalidomide is not characteristic of the usual hypnotic agents since it does not produce loss of righting reflexes or respiratory depression. Central nervous system depression produced by thalidomide can be demonstrated by its effect on spontaneous motor activity, potentiation of central depressants, and antagonism of central stimulants.

In contrast to the barbiturates, thalidomide produces a decrease in motor activity of mice in doses which do not alter motor coordination. Furthermore, it does not produce hyperactivity in low doses.

Thalidomide antagonizes the hyperactivity induced in mice by caffeine and pipradrol but is less effective against the stimulant action of d-amphetamine.

Thalidomide potentiates and prolongs the central nervous system effects of hexobarbital and barbital sodium. In some instances the potentiating effect of thalidomide is specific for certain drug actions. Thus, it potentiates the effect of anticonvulsants on maximal electroshock seizures but does not alter the acute toxicity of these drugs. It potentiates the central nervous system depressant action of chlorpromazine but does not alter significantly the dose of chlorpromazine which blocks the conditioned avoidance response.