Undergraduate Honors Theses

Thesis Defended

Spring 2016

Document Type


Type of Thesis

Departmental Honors


Psychology & Neuroscience

First Advisor

Monika Fleshner

Second Advisor

Jerry Rudy

Third Advisor

Christine MacDonald


Exercise is capable of producing a myriad of beneficial alterations in brain chemistry and function which can help prevent stress-related psychiatric disorders, such as anxiety and depression. Recent work from our lab demonstrates that 6 weeks of exercise initiated in early life produces lasting protection against stress-induced anxiety and depressive like behaviors, whereas, in adults, this protection is transient and dissipates upon cessation of exercise. Thus, when exercise begins at a young age, the neurobiological improvements remain intact even after exercise has ceased for a period of time. The mechanism underlying this long lasting protection is currently unknown. Furthermore, it is unclear which particular developmental stage is sensitive to the unique, lasting effects of exercise. The purpose of this study was to investigate the underlying mechanisms by which this long lasting stress protection occurs, as well as the developmental stage vital for producing this protection. We investigated whether early life exercise produced lasting alterations in serotonin (5-HT) 1a autoreceptor (5-HT1aR)mRNA levels; increases in mRNA for this receptor within the serotonergic dorsal raphe nucleus (DRN) are thought to be one mechanism by which exercise produces protection against the detrimental behavioral effects of stress. Juvenile, postnatal day 24 (PND 24), F344 rats ran for 6 weeks and mRNA expression levels of 5-HT1aR were measured immediately and 25 days after exercise cessation. Exercise produced persistent increases in 5-HT1aR mRNA levels within the DRN. We also investigated whether a shorter duration of exercise (3 weeks) restricted to the juvenile period could produce this unique lasting stress protection. Indeed, exercise restricted to the juvenile period produces long lasting protection against the behavioral ­consequences of stressor exposure. Further, exercise during this period increases levels of butyrate, an endogenous histone deacetylase (HDAC) inhibitor. These data suggest that lasting alterations in gene expression may underlie these behavioral effects, and that the juvenile brain may harbor exceptional traits that allow for lasting plasticity. We conjecture that exercise-induced epigenetic modifications, specifically histone acetylation, during this developmentally sensitive time are involved in this long lasting increase in 5-HT1aR mRNA. These results can inform treatments as well as prevention strategies for stress-related mental health disorders.