Northup L R
Psychopharmacology (Berl). 1976 Jul 28;48(2):189-92. doi: 10.1007/BF00423259.
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.
为了评估乙醇对小脑的作用在共济失调产生过程中的贡献，对“神经型”（nr/nr）和对照（nr/+或+/+）的C3H小鼠腹腔注射乙醇2分钟后测试其运动能力。nr/nr小鼠大部分小脑浦肯野细胞缺失。使用了两种剂量的乙醇：1.4或1.8克/千克。进行了三项运动能力测试：抓住倾斜边缘、在网格上行走和在旋转杆（跑步机）上行走。结果表明乙醇和小脑病变在共济失调产生过程中主要起累加作用。这种累加作用的可能机制是注射乙醇后浦肯野细胞活性的短暂消除。
