Pitx3 deficient mice as a genetic animal model of co-morbid depressive disorder and parkinsonism

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Title
Pitx3 deficient mice as a genetic animal model of co-morbid depressive disorder and parkinsonism
Author(s)
Kyoung Shim Kim; Y M Kang; Young Kang; Tae Shin Park; Hye Yeon Park; Y J Kim; Baek Soo Han; C H Kim; Chul Ho Lee; P A Ardayfio; P L Han; Bong Hyun Chung; K S Kim
Bibliographic Citation
Brain Research, vol. 1552, pp. 72-81
Publication Year
2014
Abstract
Approximately 40-50% of all patients with Parkinson's disease (PD) show symptoms and signs of depressive disorders, for which neither pathogenic understanding nor rational treatment are available. Using Pit3x-deficient mice, a model for selective nigrostriatal dopaminergic neurodegeneration, we tested depression-related behaviors and acute stress responses to better understand how a nigrostriatal dopaminergic deficit increases the prevalence of depressive disorders in PD patients. Pitx3-deficient mice showed decreased sucrose consumption and preference in the two-bottle free-choice test of anhedonia. Acute restraint stress increased c-Fos (known as a neuronal activity marker) expression levels in various brain regions, including the prefrontal cortex, striatum, nucleus accumbens, and paraventricular nucleus of the hypothalamus (PVN), in both Pitx3+/+ and -/- mice. However, the stress-induced increases in c-Fos levels in the cortex, dorsal striatum, and PVN were significantly greater in Pitx3-/- than +/+ mice, suggesting that signs of depressive disorders in parkinsonism are related to altered stress vulnerability. Based on these results, we propose that Pitx3-/- mice may serve as a useful genetic animal model for co-morbid depressive disorder and parkinsonism.
Keyword
c-FosDepressionParkinson's diseaseStress
ISSN
0006-8993
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/j.brainres.2014.01.023
Type
Article
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
Division of Research on National Challenges > Biodefense Research Center > 1. Journal Articles
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