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Impaired spatial performance in cerebellar-deficient Lurcher mice is not associated with their abnormal stress response

J. Tuma, Y. Kolinko, D. Jelinkova, P. Hilber, J. Cendelin,

. 2017 ; 140 (-) : 62-70. [pub] 20170214

Language English Country United States

Document type Journal Article

Both humans and laboratory animals suffering from cerebellar lesions exhibit cognitive as well as many emotional and behavioral abnormalities. These latter have been already observed in the cerebellar mutant mice currently used to highlight some aspect of autism spectrum disorders. The aim of this study was to investigate the influence of cerebellar-related stress response abnormalities on spatial learning and memory. Cerebellar-deficient Lurcher mutant mice were exposed to water environment without active escape possibility and then tested for spatial learning in the Morris water maze. As a marker of stress intensity we measured corticosterone in urine. Finally, the volumes of individual components of the adrenal gland were estimated. Though having spatial navigation deficit in the water maze, Lurcher mice preserved a substantial residuum of learning capacity. Lurcher mutants had a higher increase of corticosterone level after exposure to the water environment than wild type mice. We did not observe any decrease of this physiological stress marker between the start and the end of the spatial navigation task, despite significant improvement of behavioral performances. Furthermore, zona fasciculata and zona reticularis of the adrenal cortex as well as the adrenal medulla were larger in Lurcher mice, reflecting high stress reactivity. We conclude that for both genotypes water exposure was a strong stressor and that there was no habituation to the experiment independently to the increasing controllability of the stressor (e.g. ability to find the escape platform). Based on these findings, we suggest that the enhanced stress response to water exposure is not the main factor explaining the spatial deficits in these cerebellar mutant mice.

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$a Tuma, Jan $u Department of Pathological Physiology, Faculty of Medicine in Pilsen, Charles University, alej Svobody 1655/76, 323 00 Pilsen, Czech Republic; Laboratory of Neurodegenerative Disorders, Biomedical Center, Faculty of Medicine in Pilsen, Charles University, alej Svobody 1655/76, 323 00 Pilsen, Czech Republic.
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$a Both humans and laboratory animals suffering from cerebellar lesions exhibit cognitive as well as many emotional and behavioral abnormalities. These latter have been already observed in the cerebellar mutant mice currently used to highlight some aspect of autism spectrum disorders. The aim of this study was to investigate the influence of cerebellar-related stress response abnormalities on spatial learning and memory. Cerebellar-deficient Lurcher mutant mice were exposed to water environment without active escape possibility and then tested for spatial learning in the Morris water maze. As a marker of stress intensity we measured corticosterone in urine. Finally, the volumes of individual components of the adrenal gland were estimated. Though having spatial navigation deficit in the water maze, Lurcher mice preserved a substantial residuum of learning capacity. Lurcher mutants had a higher increase of corticosterone level after exposure to the water environment than wild type mice. We did not observe any decrease of this physiological stress marker between the start and the end of the spatial navigation task, despite significant improvement of behavioral performances. Furthermore, zona fasciculata and zona reticularis of the adrenal cortex as well as the adrenal medulla were larger in Lurcher mice, reflecting high stress reactivity. We conclude that for both genotypes water exposure was a strong stressor and that there was no habituation to the experiment independently to the increasing controllability of the stressor (e.g. ability to find the escape platform). Based on these findings, we suggest that the enhanced stress response to water exposure is not the main factor explaining the spatial deficits in these cerebellar mutant mice.
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$a Kolinko, Yaroslav $u Laboratory of Quantitative Histology, Biomedical Center, Faculty of Medicine in Pilsen, Charles University, Karlovarska 48, 301 66 Pilsen, Czech Republic; Department of Histology and Embryology, Faculty of Medicine in Pilsen, Charles University, Karlovarska 48, 301 66 Pilsen, Czech Republic.
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$a Jelinkova, Dana $u Department of Pathological Physiology, Faculty of Medicine in Pilsen, Charles University, alej Svobody 1655/76, 323 00 Pilsen, Czech Republic; Laboratory of Neurodegenerative Disorders, Biomedical Center, Faculty of Medicine in Pilsen, Charles University, alej Svobody 1655/76, 323 00 Pilsen, Czech Republic.
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$a Hilber, Pascal $u Center for Research on Psychological Function and Dysfunction, University of Rouen Normandy, Place E. Blondel, 76821 Mont saint Aignan Cedex, France.
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$a Cendelin, Jan $u Department of Pathological Physiology, Faculty of Medicine in Pilsen, Charles University, alej Svobody 1655/76, 323 00 Pilsen, Czech Republic; Laboratory of Neurodegenerative Disorders, Biomedical Center, Faculty of Medicine in Pilsen, Charles University, alej Svobody 1655/76, 323 00 Pilsen, Czech Republic. Electronic address: jan.cendelin@lfp.cuni.cz.
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