The quivering mutation arose as a spontaneous mutation in a non-inbred stock (J:167). Viability of homozygotes at weaning is normal, but life span is short, the majority dying before 5 months of age. Males are sterile, but females may be fertile and nurse their litters (J:12158). Homozygotes are characterized by locomotor instability, pronounced quivering, deafness, varying degrees of paralysis of the hindlegs, clasping of the hindlegs when held up by the tail, and priapism in most males (J:167, J:12158). Serial sections of the brain, cord, and nerve roots reveal no abnormalities, and urinary amino acids are normal (J:12160). The inner ear is histologically normal and has normal thresholds for compound action potentials at the round window. However, the thresholds for potentials in the inferior colliculus are twice as high as normal, showing that deafness, unlike that of any other deaf mutant in the mouse, is of central origin (J:11947). The raised thresholds are characteristic of all single units recorded. It is not certain whether the defect in the inferior colliculus is primary or the result of dysfunction of the superior olivary complex and lateral limniscus (J:7804). Cochlear origin distortion product otoacoustic emissions in the Spnb4^qv/Spnb4^qv mouse are normal, as might be expected in view of the central origin of deafness in this mutant (J:32693).