RESUMEN
The spastic mutant, found in the Mexican axolotl, shows swimming coordination and equilibrium deficiencies. Histological analyses of wild-type and spastic mutant cerebella previously characterized in physiological studies revealed changes in Purkinje cell location in the mutant auricle or vestibulo-cerebellum. Purkinje cells are "translocated" ventrally correlated with a similar translocation of vestibular single units described previuosly (Ide, '77). Where wild-type Purkinje cells are distributed from the surface to a depth of 250 micrometers, mutant Purkinje cells are "crowded" between 250 and 350 micrometers. Although mutant granule cells are present, boundaries between granule cell and Purkinje cell zones are less precise in mutants. Cerebellar nucleus cells are translocated medially, failing to organize into the discrete cell group appearing in wild-type. Cerebellar white matter tracts and fibers show changes, both in orientation with respect to the underlying tegmentum, and in fascicular organization. Obvious changes in the gross anatomy of the cerebellum are confirmed in reconstructions which define cell and fiber translocation. Thus, the spastic gene is compatible with differentiation of all cerebellar elements, but appears to alter interactions between cells, or between cells and the external milieu. Although all cell types are present in the mutant cerebellum, they fail to attain their proper positions along all three body axes.
Asunto(s)
Ambystoma/genética , Cerebelo/anatomía & histología , Mutación , Células de Purkinje , Animales , Ratones/genéticaRESUMEN
The homozygous recessive spastic mutant found in the Mexican axolotl shows violent coiling and thrashing behavior when subjected to strong tactile or electrical stimulation. In order to establish the time of onset of the first behavioral manifestation of the spastic gene, an etiological analysis of the ontogeny of swimming behavior in mutants and wild type siblings was undertaken. The locomotor patterns shown by embryos in response to an electrical stimulus were analyzed quantitatively from the embryonic early flexure stage through the larval early feeding stage. Spastic larvae failed to show dorsal-up swimming frequencies equal to those of sibling controls from day 12 (Harrison stage 40) of development indicating a lack of equilibrium. Both spastics and their siblings showed "sinusoid swimming" and "coiling" behavior in response to an aversive stimulus through day 18 (Harrison state 46, early feeding stage) of development. From day 18, wild type siblings abruptly decreased "coiling" behavior and showed strong "escape swimming" in response to an intense stimulus. Spastics never developed "escape swimming" patterns but retained a mixture of "sinusoid swimming" and "coiling" patterns characteristic of pre-feeding stage larvae.