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Abstract
Lurcher mutant mice represent a natural model of olivocerebellar degeneration. This
degeneration is caused by a mutation of the gene for the delta2 glutamate receptor.
Lurcher mutants suffer from cerebellar ataxia and cognitive functions deficiency as
a consequence of excitotoxic apoptosis of Purkinje cells in the cerebellar cortex
and a secondary decrease of granule cells and inferior olive neurons. This process
finishes by the 90th day of postnatal life, but already by 14 days, the Purkinje cells
are damaged and the ataxia is fully developed. Purkinje cells die by apoptosis within
the first 3 weeks of life. The aim of our work was to study the development of motor
functions in the course of the ontogenetic development in Lurcher mutant mice of the
B6CBA strain and to compare it with wild type mice of the same strain. Mice aged 2,
3, 6, 9, and 22 weeks were used in our experiment. Motor skills were examined using
four standard tests: the horizontal wire, rotating cylinder, footbridge and slanting
ladder. Our findings in Lurcher mutant mice show a significant increase of motor abilities
up to the sixth postnatal week and selective decrease early after this period. This
improvement of motor skills is caused by the physiological development of musculature
and the nervous system, probably with some contribution of plasticity of the maturing
brain. The cause of the decline of these abilities immediately after the completion
of the development is unknown.