Abstract
In order to assess the contribution of cerebellar effects of ethanol to the production of ataxia, “nervous” (nr/nr) and control (nr/+ or +/+) C3H mice were tested for locomotor ability 2 min after being given intraperitoneal ethanol injections. The nr/nr mice suffer from loss of most of their cerebellar Purkinje cells. Two doses of ethanol were used: 1.4 or 1.8 g/kg. There were three tests of locomotor ability: holding onto a tilting edge, grid walking, and Rota-rod (treadmill) walking. The result sindicate a primarily additive effect of ethanol and cerebellar pathology in the production of ataxia. The probable mechanism of this additive effect is the transient elimination of Purkinje cell activity following an ethanol injection.