作者: Mmalebuso L. Mokoena , Brian H. Harvey , Francois Viljoen , Susanna M. Ellis , Christiaan B. Brink
DOI: 10.1007/S00213-015-3928-8
关键词:
摘要: Major depression has been associated with higher levels of air pollution that in turn leads to neurodegeneration via increased oxidative stress. There is a need for suitable translational animal models study the role stress and antidepressant action. Considering gene X environment hypothesis depression, present investigated effect chronic ozone inhalation on anxiety-related behavior, cognition, brain markers Flinders Sensitive Line (FSL) rat. In addition, response antioxidant melatonin, antidepressants desipramine or escitalopram, was assessed. Rats were exposed (0.0 0.3 parts per million (ppm)) 4 h daily period 15 days, while simultaneously receiving saline above-mentioned drugs. The data indicate induced memory impairment, anxiety depression-like effects, reduced cortical hippocampal superoxide dismutase catalase activity, compromised central monoamine similar noted depression. Moreover, behavioral neurochemical effects desipramine, escitalopram mostly attenuated presence ozone. Thus, genetically susceptible individuals high are at risk developing mood and/or an disorders, showing greater redox imbalance altered behavior. These animals also more resistant contemporary treatment. presented model provides robust face, construct, predictive validity, studying neuronal action mechanisms prevent