A new neurological mutant (creeping) rat : genetic and some neuropathological aspects.

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We have found a new mutant rats, named creeping, that exhibits severe ataxia. The affected rats are recognized at 15 days and die within 35 days. In the 21-day-old mutant there is a remarkable cerebellar hypoplasia accompanied with malpositioning of neurons both in cerebella and cerebra. There are no sex differences in the phenotype. The genetic study suggest that the creeping traits caused by an autosonal recessive gene.The creeping rats can be predicted by crooked tail prior to the neurological signs. Study of alizarin-stained skeletons showed great reduction in number and misalignments of the tail vertebrae. Linkage tests of crooked tail, symbolized crt, located it extremely close to creeping, cre(recombinant value : 0.127<plus-minus>0.129The mutant cerebelluir had a few rudimentary folia with disorganized tissue architecture in terms of neuronal positioning. The cerebellar lamination was severely disturbed even on 28 days in the mutant, although a typical tri-liniar structure was already present on 21 days in the normal. Inner granular neurons were markedly reduced in number and Purkinie cells were deeply located, i. e., in the vicinity of the white matter. Purkinie cells were scattered among the maldeveloped inner granule layer as well. GFAP-positive cells increased in number in the mutant cerebellum as compared with the normal one at 21 days. They were located among granular neurons and Purkinie cells. Processes of GFAP-positive cells were thick and irregularly branched. However, these processes be came slender in the 28-day-old mutant cerebellum.The creeping rat not only provide a valuable system where the neuronal migration is analyzed but may also give us a clue to elucidate. the functions of the GFAP-positive cells during development.