Jolting mice carry a spontaneous, autosomal recessive mutation characterized by cerebellar ataxia and generalized tremor and exhibit progressive weakness due to a functional denervation of skeletal muscle. The mutation results in substitution of Thr for an evolutionarily conserved Ala residue in the cytoplasmic S4-S5 linker of domain III. Abnormalities in the cerebellum are responsible for the gait problems of the jolting mouse, and preliminary morphological and neurophysiological examination of the mouse with motor end-plate disease has shown that it also has cerebellar abnormalities. Axonal spheroids may be seen on cerebellar Purkinje cell axons, and the character of extra-cellular recordings obtained from the Purkinje cells is abnormal.

Jolting mice carry a spontaneous, autosomal recessive mutation characterized by cerebellar ataxia and generalized tremor and exhibit progressive weakness due to a functional denervation of skeletal muscle attributed to abnormalities in the cerebellum.

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