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首页> 外文期刊>The European Journal of Neuroscience >Increased adult hippocampal neurogenesis is not necessary for wheel running to abolish conditioned place preference for cocaine in mice
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Increased adult hippocampal neurogenesis is not necessary for wheel running to abolish conditioned place preference for cocaine in mice

机译：成年海马神经发生的增加对于滚轮行驶消除小鼠的可卡因条件性位置偏爱不是必需的

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Recent evidence suggests that wheel running can abolish conditioned place preference (CPP) for cocaine in mice. Running significantly increases the number of new neurons in the hippocampus, and new neurons have been hypothesised to enhance plasticity and behavioral flexibility. Therefore, we tested the hypothesis that increased neurogenesis was necessary for exercise to abolish cocaine CPP. Male nestin-thymidine kinase transgenic mice were conditioned with cocaine, and then housed with or without running wheels for 32days. Half of the mice were fed chow containing valganciclovir to induce apoptosis in newly divided neurons, and the other half were fed standard chow. For the first 10days, mice received daily injections of bromodeoxyuridine (BrdU) to label dividing cells. On the last 4days, mice were tested for CPP, and then euthanized for measurement of adult hippocampal neurogenesis by counting the number of BrdU-positive neurons in the dentate gyrus. Levels of running were similar in mice fed valganciclovir-containing chow and normal chow. Valganciclovir significantly reduced the numbers of neurons (BrdU-positive/NeuN-positive) in the dentate gyrus of both sedentary mice and runner mice. Valganciclovir-fed runner mice showed similar levels of neurogenesis as sedentary, normal-fed controls. However, valganciclovir-fed runner mice showed the same abolishment of CPP as runner mice with intact neurogenesis. The results demonstrate that elevated adult hippocampal neurogenesis resulting from running is not necessary for running to abolish cocaine CPP in mice.
机译：最近的证据表明，轮转可以消除小鼠中可卡因的条件位置偏爱（CPP）。跑步会显着增加海马中新神经元的数量，并且已假设新神经元可增强可塑性和行为灵活性。因此，我们检验了以下假设：增加运动对于消除可卡因CPP是必要的。用可卡因使雄性巢蛋白-胸苷激酶转基因小鼠适应，然后在有或没有转轮的情况下饲养32天。一半的小鼠被喂食含有缬更昔洛韦的食物以诱导新分裂的神经元的凋亡，另一半被喂食标准食物。在最初的10天里，小鼠每天注射溴脱氧尿苷（BrdU）来标记分裂细胞。在最后四天，对小鼠进行CPP测试，然后通过计数齿状回中BrdU阳性神经元的数量来安乐死以测量成年海马神经发生。用含缬更昔洛韦的食物和正常食物喂养的小鼠的跑步水平相似。 Valganciclovir大大减少了久坐小鼠和奔跑小鼠的齿状回中神经元的数量（BrdU阳性/ NeuN阳性）。用Valganciclovir喂养的跑步小鼠表现出与久坐，正常喂养的对照组相似的神经发生水平。然而，用缬更昔洛韦喂养的流浪小鼠显示出与具有完整神经发生的流浪小鼠相同的CPP废除。结果表明，奔跑引起的成年海马神经发生对于奔跑消除小鼠中的可卡因CPP并不是必需的。

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