| Background: Stroke is a nervous system disease with high morbidity,high mortality and high disability rate, which seriously affects people’shealth and living quality. It has been confirmed that exercise could promoteneurological rehabilitation and neuronal plasticity in patients with stroke.However, the exact mechanisms have not been fully explained. So it isnecessary to study the mechanism. Serotonin is an importantneurotransmitter in central nervus system, which is related with neuronalplasticity. This study focuses on5-HT to implore the mechanism ofexercise-induced neuronal plasticity.Objective: To discuss the effects of treadmill exercises on scores ofneurological function, contents of5-HT, expressions of5-HT1A receptor,BDNF and synaptophysin in hippocampus and cortex of rats afterpermanent middle cerebral artery occlusion(pMCAO).Methods: A total of85rats were randomly divided into three groups:pMCAO group (n=30), pMCAO and treadmill exercise (pMCAO+Ex)group (n=25) and sham-operated group (n=30). Middle cerebral artery occlusion (MCAO) method was used to establish focal permanent cerebralinfarction model. Rats in pMCAO+Ex group underwent treadmill exerciseon the3rd day after model establishment for16days. Neurologicalfunction was evaluated using modified neurological severity scores(mNSS). HE staining and nissel staining were used to observe neurondamages in CA2region of hippocampus and cortex. High performanceliquid chromatography-electrochemical detection system was used todetermine levels of5-HT in ischemia hippocampus and cortex tissues.mRNA levels of5-HT1A receptor were determined by reversetranscription-polymerase chain reaction. Protein levels of5-HT1A receptor,BDNF and synaptophysin in hippocampus and cortex were measured byWestern blot.Results: mNSS was lower in pMCAO+Ex group than in pMCAOgroup on the19th day post MCAO (p<0.001). Both stainings showed thatthe morphologies of neurons in CA2region and cortex were normal insham-operated group and irregular in pMCAO group with parts of neuronsbeing obviously damaged; after treadmill exercise, the damage wasalleviated. Contents of hippocampus5-HT was higher in pMCAO+Exgroup (14.5±1.71) ng/ml than in pMCAO group (7.13±0.71) ng/ml(p<0.001). Contents of cortex5-HT dropped to3.81±1.86ng/ml inpMCAO group (43.84±2.05ng/ml in sham-operated group), and increasedin pMCAO+Ex group (10.06±1.80ng/ml). Protein and mRNA expressions of5-HT1A receptor and protein expressions of synaptophysin inhippocampus were upregulated after treadmill exercise comparing withthose in pMCAO group (p<0.05). The protein expression of synaptophysin,5-HT1A receptor and BDNF in cortex were downregulated after cerebralinfarction (p<0.05), and upregulated after treadmill exercise (p<0.05).Conclusions: Treadmill exercises could improve neurologicalfunction, increase contents of5-HT and levels of5-HT1A receptor inhippocampus, upregulate the levels of5-HT,5-HT1A receptor and BDNFin cortex to improve synaptic plasticity. |
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