David Marriott, Brigham Young University
Physiology and Developmental Biology
Acute stress has been shown to decrease Long-Term Potentiation (LTP) in the CA1 region of the mouse hippocampus. Additionally, stressed animals show signs of anxiety and suffer decreases in spatial memory tasks such as object recognition and maze navigation. Conversely, exercise has been shown to increase spatial memory task performance in mice, attenuate anxiety-like behaviors and enhance neurogenesis and LTP in the dentate gyrus. While the effects of stress and exercise have been examined independently, there is currently a lack of experimental evidence that connects how stress and exercise, when experienced by the same animal, might modulate LTP in the CA1 region of the hippocampus. In our ongoing study, mice have been separated into a control group, a stress group (restraint and tail-shock), and an exercise + stress group where mice have voluntary access to a running wheel (for 30 days) before undergoing the stress protocol. We hypothesize that exercised animals will experience a protective effect against the reductions in CA1 LTP. In the stress only group, preliminary data shows a modest stress effect on LTP, yet we are learning that factors such as controllability of the stressor or the ability to develop coping mechanisms might potentially attenuate
the decreases in LTP due to stress. Additionally, the axis on which brain dissection takes place appears to be a significant factor, one in which previous studies have failed to specify, as the dorsal and ventral hippocampus display opposite neuronal adaptations to stress. We will begin experimentation soon with the stress + exercise group which will provide additional data to further our discussion of the means by which various behaviors might modulate LTP in stressed animals.