Effects of Exercise on Learning and Memory Performance of Rats Undergoing Nicotine Withdrawal and Its Underlying Mechanism / 中国运动医学杂志

ABSTRACT

Objective To explore the impact of exercise on the learning and memory of rats undergoing nicotine withdrawal and its underlying mechanism.Methods Forty four-week-old male SpragueDawley rats were subjected to nicotine conditioned place preference(CPP) training before being randomly separated into a high-,moderate-,low-intensity exercise and control(no exercise) group.Rats in exercise groups underwent the treadmill running at low,moderate or high intensity 30 minutes per day for 10 days consecutively.The nicotine-associated context memory was evaluated using the CPP preference score.Morris water maze (MWM) tasks were used to examine the spatial learning and memory.The protein level of α7 acetylcholine receptors(nAChRs) in the prefrontal cortex and hippocampus was visualized by Western blotting.Results Rats undergoing exercises at a high or moderate intensity had a significantly lower CPP score than the control group (P＜0.01 and P＜0.05 respectively).However,there was no significant difference in the CPP score between the low-intensity exercise and control groups.Only rats doing moderate-intensity exercise presented a significantly shorter escape latency than controls in the MWM place navigation test(P＜0.01).Significant increase in time spent and distance swam in the target quadrant was observed in the moderate-and high-intensity exercise group,but without significant differences between the two groups.Moreover,a significant increase in the number of crossing target quadrant was only observed in rats that exercised at a moderate intensity (P＜ 0.05).The protein level of α7 nAChRs was significantly elevated in the prefrontal cortex(P＜0.01),but not in the hippocampus of rats doing moderate intensity exercise.Conclusion Ten-day treadmill running at a moderate intensity may improve learning and memory performance,and facilitate the extinction of nicotine reward memory of nicotine-treated rats via increasing α7 nAChR-mediated signaling in the frontal cortex.