Departamento de Fisiologia, Universidade Federal de São Paulo/Escola Paulista de Medicina (UNIFESP/EPM), São Paulo, SP, Brazil.
J Neurochem. 2015 Jan;132(2):206-17. doi: 10.1111/jnc.12976. Epub 2014 Nov 17.
Physical exercise stimulates the release of endogenous opioid peptides supposed to be responsible for changes in mood, anxiety, and performance. Exercise alters sensitivity to these effects that modify the efficacy at the opioid receptor. Although there is evidence that relates exercise to neuropeptide expression in the brain, the effects of exercise on opioid receptor binding and signal transduction mechanisms downstream of these receptors have not been explored. Here, we characterized the binding and G protein activation of mu opioid receptor, kappa opioid receptor or delta opioid receptor in several brain regions following acute (7 days) and chronic (30 days) exercise. As regards short- (acute) or long-term effects (chronic) of exercise, overall, higher opioid receptor binding was observed in acute-exercise animals and the opposite was found in the chronic-exercise animals. The binding of [(35) S]GTPγS under basal conditions (absence of agonists) was elevated in sensorimotor cortex and hippocampus, an effect more evident after chronic exercise. Divergence of findings was observed for mu opioid receptor, kappa opioid receptor, and delta opioid receptor receptor activation in our study. Our results support existing evidence of opioid receptor binding and G protein activation occurring differentially in brain regions in response to diverse exercise stimuli. We characterized the binding and G protein activation of mu, kappa, and delta opioid receptors in several brain regions following acute (7 days) and chronic (30 days) exercise. Higher opioid receptor binding was observed in the acute exercise animal group and opposite findings in the chronic exercise group. Higher G protein activation under basal conditions was noted in rats submitted to chronic exercise, as visible in the depicted pseudo-color autoradiograms.
体育锻炼会刺激内源性阿片肽的释放，这些肽被认为负责调节情绪、焦虑和表现。运动改变了这些影响的敏感性，从而改变了阿片受体的效力。虽然有证据表明运动与大脑中的神经肽表达有关，但运动对阿片受体结合和这些受体下游的信号转导机制的影响尚未得到探索。在这里，我们在急性（7 天）和慢性（30 天）运动后，对几个脑区的μ阿片受体、κ阿片受体或δ阿片受体的结合和 G 蛋白激活进行了特征描述。关于运动的短期（急性）或长期（慢性）效应，总的来说，急性运动动物的阿片受体结合更高，而慢性运动动物则相反。在感觉运动皮层和海马体中，（35）S]GTPγS 在基础条件下（无激动剂）的结合增加，这种效应在慢性运动后更为明显。在我们的研究中，μ阿片受体、κ阿片受体和δ阿片受体受体激活的发现存在分歧。我们的结果支持了现有的证据，即阿片受体结合和 G 蛋白激活在不同的运动刺激下在大脑区域中发生不同。我们在急性（7 天）和慢性（30 天）运动后，对几个脑区的μ、κ和δ阿片受体的结合和 G 蛋白激活进行了特征描述。急性运动动物组观察到较高的阿片受体结合，而慢性运动组则相反。在慢性运动大鼠中，基础条件下的 G 蛋白激活更高，如图所示的伪彩色放射自显影所示。
