Abstract

Cell damage and cell generation can be altered in a stressed and exercised brain. However, it is not known whether voluntary exercise can prevent cell damage or cell death in stress situations, especially in the striatal region. To address this question, male Sprague-Dawley rats (3 months old) were separated into three groups (sedentary, restraint stress, and voluntary exercise+ restraint stress groups). The stress circumstances were restraint stress, light stress, and tilt cage. To assess cell damage, staining for the heat shock protein (HSP90) was undertaken and the numbers of cells showing positive HSP90 expression were counted. Neurogenesis was investigated by staining for nestin markers. The restraint stress effects were assessed by determining the number of HSP90 expressed cells produced in the dorsal striatum. A significant difference was found when the number of HSP90 positive cells in the restraint stress and the voluntary exercise+ restraint stress groups were compared to those in the sedentary control group. In both experimental conditions there was neurogenesis in the striatal area. However, the group that received voluntary exercise presented a significantly higher number of nestin-expressing cells over the restraint stress group. Voluntary exercise might have an adaptive effect on neurogenesis in terms of replenishing the cellular stressed neurons but it has no effect on ameliorating the level of stress marker. The evaluation of the effects of voluntary exercise on neurogenesis in the striatal region in the stressed model might contribute to a better understanding of beneficial interventions in movement disorders related to patients with depression.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.