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首页> 外文期刊>Brain research >Elevated dopamine levels during gestation produce region-specific decreases in neurogenesis and subtle deficits in neuronal numbers.
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Elevated dopamine levels during gestation produce region-specific decreases in neurogenesis and subtle deficits in neuronal numbers.

机译：妊娠期间多巴胺水平升高会导致神经发生区域特异性降低和神经元数量微不足道。

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摘要

Dopamine levels in the fetal brain were increased by administering the dopamine precursor 3,4-dihydroxy-l-phenylalanine (l-DOPA) to pregnant mice in drinking water. The l-DOPA exposure decreased bromodeoxyuridine (BrdU) labeling in the lateral ganglionic eminence and frontal cortical neuroepithelium but not medial or caudal ganglionic eminences. The regional differences appear to reflect heterogeneity in precursor cells' responses to dopamine receptor activation. Relative numbers of E15-generated neurons were decreased at postnatal day 21 (P21) in the caudate-putamen, nucleus accumbens and frontal cortex but not globus pallidus in the l-DOPA group. TUNEL labeling did not show significant differences on P0, P7 or P14 in the caudate-putamen or frontal cortex, suggesting that cell death was not altered. Although virtually all cells in the P21 brains that were labeled with the E15 BrdU injection were NeuN-positive, stereological analyses showed no significant changes in total numbers of NeuN-positive or NeuN-negative cells in the P21 caudate-putamen or frontal cortex. Thus persisting deficits in neuronal numbers were evident in the l-DOPA group only by birth-dating analyses and not upon gross histological examination of brain sections or analysis of total numbers of neurons or glia. One explanation for this apparent discrepancy is that l-DOPA exposure decreased cell proliferation at E15 but not at E13. By E15, expansion of the neuroepithelial precursor pool is complete and any decrease in cell proliferation likely produces only marginal decreases in the total numbers of cells generated. Our l-DOPA exposure model may be pertinent to investigations of neurological dysfunction produced by developmental dopamine imbalance.
机译：通过给饮用水中的怀孕小鼠服用多巴胺前体3,4-二羟基-1-苯丙氨酸（1-DOPA），可以增加胎儿大脑中的多巴胺水平。 I-DOPA暴露可减少外侧神经节隆起和额皮质神经上皮中的溴脱氧尿苷（BrdU）标记，但不会降低内侧或尾神经节隆起。区域差异似乎反映了前体细胞对多巴胺受体激活的反应的异质性。出生后第21天（P21），尾巴-丘脑，伏伏核和额叶皮层中E15产生的神经元的相对数目减少，而1-DOPA组则无苍白球。 TUNEL标记在尾状丘脑或额叶皮层的P0，P7或P14上未显示出显着差异，表明细胞死亡未改变。尽管实际上用E15 BrdU注射标记的P21脑中的所有细胞均为NeuN阳性，但立体分析显示，P21尾状丘脑或额叶皮层中NeuN阳性或NeuN阴性细胞的总数没有显着变化。因此，仅通过出生日期分析，而不是通过对脑切片的总体组织学检查或对神经元或神经胶质细胞总数的分析，在l-DOPA组中神经元数量的持续缺陷才是明显的。这种明显差异的一种解释是1-DOPA暴露会降低E15处的细胞增殖，但不会降低E13处的细胞增殖。到E15时，神经上皮前体池的扩增完成，细胞增殖的任何减少都可能仅使产生的细胞总数略有减少。我们的l-DOPA暴露模型可能与发育性多巴胺失衡所引起的神经功能障碍的研究有关。

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