...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The European Journal of Neuroscience >Chronic cocaine exposure impairs progenitor proliferation but spares survival and maturation of neural precursors in adult rat dentate gyrus.
【24h】

Chronic cocaine exposure impairs progenitor proliferation but spares survival and maturation of neural precursors in adult rat dentate gyrus.

机译：慢性可卡因暴露会损害祖细胞的增殖，但会保留成年大鼠齿状回的神经前体的存活和成熟。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Recent observations indicate that drugs of abuse, including alcohol and opiates, impair adult neurogenesis in the hippocampus. We have studied in rats the impact of cocaine treatment (20 mg/kg, daily, i.p.) on cell proliferation, survival and maturation following short-term (8-day) and long-term (24-day) exposure. Using 5'-bromo-2-deoxyuridine (BrdU) and Ki-67 as mitotic markers at the end of the drug treatments, we found that both short- and long-term cocaine exposures significantly reduced cell proliferation in the dentate gyrus (DG) of the hippocampus. By labelling mitotic cells with BrdU pulses before or during the early stages of the drug treatment, we determined that long-term cocaine exposure did not affect the survival of newly generated cells. In register with this finding, cocaine chronic exposure did not increase the number of apoptotic cells labelled by TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling). Using doublecortin (DCX) immunocytochemistry and electron microscopy, we next examined the effects of cocaine exposure on the maturation of the neural precursors and on synaptic output to CA3. DCX immunocytochemistry showed that immature hippocampal cells of rats exposed to cocaine displayed normal arborization patterns and similar degrees of colocalization with BrdU at two different developmental stages. Moreover, cocaine did not produce significant morphological alterations of the mossy fibre projection system to stratum lucidum in the CA3 area of the hippocampus. The results presented demonstrate that chronic cocaine exposure impairs proliferation dynamics in the DG without significantly altering either the survival and growth of immature cells or the structural features of terminal projections to CA3.
机译：最近的观察表明，滥用药物，包括酒精和鸦片制剂，会损害海马的成年神经发生。我们已经在大鼠中研究了可卡因治疗（20 mg / kg，每天，腹腔注射）对短期（8天）和长期（24天）暴露后细胞增殖，存活和成熟的影响。在药物治疗结束时使用5'-溴-2-脱氧尿苷（BrdU）和Ki-67作为有丝分裂标记物，我们发现短期和长期可卡因暴露均显着降低了齿状回（DG）中的细胞增殖。海马。通过在药物治疗之前或之前用BrdU脉冲标记有丝分裂细胞，我们确定长期可卡因暴露不会影响新产生细胞的存活。与该发现相吻合的是，可卡因的长期暴露并未增加通过TUNEL（末端脱氧核苷酸转移酶介导的dUTP缺口末端标记）标记的凋亡细胞的数量。使用双皮质素（DCX）免疫细胞化学和电子显微镜，我们接下来检查了可卡因暴露对神经前体成熟以及对CA3的突触输出的影响。 DCX免疫细胞化学显示，暴露于可卡因的大鼠未成熟海马细胞在两个不同的发育阶段表现出正常的乔化模式和与BrdU相似的共定位程度。此外，可卡因并未在海马CA3区的苔藓纤维投射系统向透明层形成明显的形态学改变。提出的结果表明，长期可卡因暴露会损害DG中的增殖动力学，而不会显着改变未成熟细胞的存活和生长或未向CA3末端突出的结构特征。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号