Abstract
Using the R6/1 mouse model of Huntington disease (HD), we have recently shown that voluntary physical activity was able to correct the depressive-like behaviours exhibited by the HD animals at a pre-motor symptomatic stage of the disease. Using the high performance liquid chromatography system, we have now evaluated the effect of exercise on monoamine metabolism in HD mice. We found that serotonin and its metabolite as well as dopamine and noradrenaline were reduced across several brain regions in female R6/1 animals. Our data also suggest that some of these neurochemical deficits were modulated by physical activity, in a genotype-region dependent manner. These newly identified changes could account for some of the behavioural effects of exercise previously reported in HD mice.
Highlights
Huntington disease (HD) is an autosomal dominant neurodegenerative disorder caused by expansion of CAG repeats in exon 1 of the huntingtin gene [1]
Alterations in 5-HT and/or DA systems have been found in pre-motor symptomatic R6 HD animals[6] [7] [8] [14] [15], and we have recently shown that the associated depressive-like behaviours exhibited by R6/1 female mice were corrected by chronic treatment with the serotonin reuptake inhibitor (SSRI) sertraline as well as voluntary physical activity[7]
Similar significant deficits of the metabolite 5-hydroxyindolacetic acid (5-HIAA) were displayed by HD animals in all brain regions studied (Figure 1 and Table 1)
Summary
Huntington disease (HD) is an autosomal dominant neurodegenerative disorder caused by expansion of CAG repeats in exon 1 of the huntingtin gene [1]. Clinical onset of HD is determined on the basis of motor symptoms; the pre-motor stages of the disease are commonly associated with cognitive deficits as well as psychiatric manifestations such as depression[2] [3] [4] [5]. Alterations in 5-HT and/or DA systems have been found in pre-motor symptomatic R6 HD animals[6] [7] [8] [14] [15], and we have recently shown that the associated depressive-like behaviours exhibited by R6/1 female mice were corrected by chronic treatment with the serotonin reuptake inhibitor (SSRI) sertraline as well as voluntary physical activity[7]
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