作者: Christina Mo , Thibault Renoir , Anthony J. Hannan
DOI: 10.1016/J.BBR.2014.07.044
关键词:
摘要: Abstract Huntington's disease (HD) is an autosomal dominant, neurodegenerative disorder with cognitive, psychiatric, motor, neuroendocrine and peripheral dysfunctions. Symptom onset progression can be closely modeled in HD transgenic mice, which facilitate the search for therapeutics environmental modulators. In first investigation of chronic stress HD, we have previously shown that administering a moderate dose hormone, corticosterone (CORT) had no effect on short-term memory wildtype (WT) mice but accelerated impairment male R6/1 mice. We now extend this to ethological dysfunctions hypothesized more susceptible CORT treatment compared same functions WT littermates. Both genotypes consumed similar doses dissolved drinking water across 6–14 weeks age were assessed olfactory sensitivity, nest-building, saccharin preference as well vocal responses sociosexual stimuli. female sensitivity reduced by 2 4 CORT, respectively. males, there was preference, however number vocalizations mouse transiently increased CORT-drinking, regardless genotype. Nest-building severely impaired at early age, unaffected CORT. Our results suggest presence mutation bearing CORT-induced effects dose, suggesting even moderately elevated hormone levels impair behaviors both healthy brain.