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National Repository of Grey Literature 2 records found  Search took 0.00 seconds. 
Circadian system and it's changes in Lurcher mutant mice
 Boubín, Josef ; Bendová, Zdeňka (advisor) ; Jelínková, Dana (referee)
The main topic of this thesis are changes in Circadian rhythms caused by cerebellar disorders. Mice with Lurcher mutation, which have specifically degenerated Purkinje cells layer, were choosen as animal model. Our results show that mutation of the glutamate receptor GluRδ2, which causes gradual degeneration of Purkinje cells, leads to damage of Circadian system. Mice with this mutation have reduced capability to adapt to external conditions in different light modes. They are also showing increased variability in endogenous cycle. The mice are also unable to show anticipatory behavior in time-restricted feeding. Compared to control group, affected mice do not show significant rhythm in levels of protein of Bmal1 gene in suprachiasmatic nuclei, paraventricular nuclei nor in habenula. Phosphorylated kinases ERK1/2 and GSK3ß also had distorted rhythms in suprachiasmatic nuclei. Because Circadian oscillations in locomotor activity are partly preserved, Circadian system is likely not damaged on molecular level. Cerebellar mutation hampers synchronization between suprachiasmatic nuclei of neurons and can also affect processes in the ventromedial hypothalamus regulating food intake. Our findings are the first to suggest functional interactions between cerebellum and Circadian pacemaker in suprachiasmatic...
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Characteristics of the nervous system of mice with a Lurcher mutation
 Boubín, Josef ; Bendová, Zdeňka (advisor) ; Tůma, Jan (referee)
The glutamate receptor δ 2 (GluRδ2) is expressed in dendrites of Purkinje cells localized in the cerebellar cortex. Correct function of GluRδ2 is necessary for cerebellar development, synapse formation between parallel fibers of the granular and Purkinje cells and for inducing long term depression important in memory formation. Lurcher mutation, localized to 6th autosomal chromosome, transforms GluRδ2 into constitutively open ion channel by amino acid substitution in third transmembrane domain. As a result, almost complete disappearance of Purkinje cells population and a large degeneration of granular cells and olivary neurons occurs. Mice impaired by Lurcher mutation have lower body weight and reduced litter size. Fertility of males is not affected. Lurcher mutants display extensive behavioral deficits. Mice suffer from ataxia typical for cerebellar neurodegenerations. They have reduced physical performance, impaired spatial orientation and learning capabilities. The aim of this work is to summarize recent knowledge about Lurcher mutation from molecular basis to behavioral manifestation. Specific characteristics of this degeneration allow us to investigate influences of neurodegenerative cerebellar disorders on cognitive functions of the brain as a whole, study causing factors and treatment...
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