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首页> 外文期刊>The European Journal of Neuroscience >Increased extracellular dopamine concentrations and FosB/DeltaFosB expression in striatal brain areas of heterozygous GDNF knockout mice.
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Increased extracellular dopamine concentrations and FosB/DeltaFosB expression in striatal brain areas of heterozygous GDNF knockout mice.

机译：杂合的GDNF基因敲除小鼠的纹状体脑区域中的细胞外多巴胺浓度和FosB / DeltaFosB表达增加。

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Glial cell line-derived neurotrophic factor (GDNF) has been shown to be involved in the maintenance of striatal dopaminergic neurons. To study whether reduced levels of endogenous GDNF affect the striatal dopaminergic transmission we estimated the basal extracellular levels of dopamine in vivo, the basal expression of FosB-related proteins in striatal brain areas as well as the effects of acute and repeated cocaine on locomotor activity and dopamine output in mice lacking one GDNF allele (heterozygous GDNF+/- mice). As expected the striatal GDNF protein content was found to be smaller in the GDNF+/- mice than in their wild-type littermates. Unexpectedly the extracellular dopamine concentration in the GDNF+/- mice in the dorsal striatum (CPu) was 2.0-fold, and in the nucleus accumbens (NAc) 1.6-fold the concentration found in the wild-type littermates. Also FosB/DeltaFosB-like immunoreactivity was found to be elevated in the CPu as well as in the core and in the shell of NAc of the GDNF+/- mice as compared with the wild-type mice. This suggests chronic postsynaptic activation of these brain areas and is in line with elevated extracellular dopamine concentrations. Cocaine's effects acutely and after repeated treatment on locomotor activity were similar in the GDNF+/- and the wild-type mice. Neither did cocaine's acute effects on dopamine output differ between the mice of the two strains. Our findings demonstrate that reduced levels of endogenous GDNF induce alterations in dorsal striatal and accumbal dopaminergic transmission, and stress the importance of endogenous GDNF in the regulation of the dopaminergic neurons.
机译：胶质细胞源性神经营养因子（GDNF）已被证明参与纹状体多巴胺能神经元的维持。为了研究内源性GDNF水平降低是否会影响纹状体多巴胺能传递，我们估算了体内多巴胺的基础细胞外水平，纹状体脑区域中FosB相关蛋白的基础表达以及急性和反复可卡因对运动能力的影响。缺乏一个GDNF等位基因的小鼠（杂合GDNF +/-小鼠）的多巴胺输出。如预期的那样，发现GDNF +/-小鼠的纹状体GDNF蛋白含量比其野生型同窝仔动物小。出乎意料的是，背侧纹状体（CPu）的GDNF +/-小鼠中的细胞外多巴胺浓度是野生型同窝鼠中的2.0倍，伏隔核（NAc）中是1.6倍。还发现与野生型小鼠相比，GDNF +/-小鼠的CPu以及NAc的核心和外壳中的FosB / DeltaFosB样免疫反应性均升高。这表明这些大脑区域的慢性突触后激活，并与升高的细胞外多巴胺浓度相一致。在GDNF +/-和野生型小鼠中，可卡因的急性作用和反复治疗后对运动活性的作用相似。可卡因对多巴胺输出的急性影响在两种品系的小鼠之间也没有不同。我们的发现表明，内源性GDNF水平降低会诱导背纹状体和伏隔多巴胺能传递的改变，并强调内源性GDNF在调节多巴胺能神经元中的重要性。

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