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烟草烟雾会减少青少年大鼠齿状回中的神经发生并促进神经胶质增生。

Tobacco smoke diminishes neurogenesis and promotes gliogenesis in the dentate gyrus of adolescent rats.

机构信息

Department of Psychiatry, College of Medicine, McKnight Brain Institute, University of Florida, 100 S. Newell Dr., Gainesville, FL 32610, USA.

出版信息

Brain Res. 2011 Sep 21;1413:32-42. doi: 10.1016/j.brainres.2011.07.041. Epub 2011 Jul 24.

DOI:10.1016/j.brainres.2011.07.041
PMID:21840504
Abstract

Brain disorders and environmental factors can affect neurogenesis and gliogenesis in the hippocampus. These studies investigated the effects of chronic exposure to tobacco smoke on progenitor cell proliferation and the survival and phenotype of new cells in the dentate gyrus of adolescent rats. The rats were exposed to tobacco smoke for 4h/day for 14 days. To investigate cell proliferation, the exogenous marker 5-bromo-2'-deoxyuridine (BrdU, 200mg/kg, ip) was administered 2h into the 4-h smoke exposure session on day 14. The rats were sacrificed 2-4h after the administration of BrdU. To investigate cell survival, the same dose of BrdU was administered 24h before the start of the 14-day smoke exposure period. These rats were sacrificed 24h after the last smoke exposure session. Tobacco smoke exposure decreased both the number of dividing progenitor cells (-19%) and the number of surviving new cells (-20%), labeled with BrdU in the dentate gyrus. The decrease in cell proliferation was not associated with an increase in apoptotic cell death, as shown by TUNEL analysis. Colocalization studies indicated that exposure to tobacco smoke decreased the number of new immature neurons (BrdU/DCX-positive) and transition neurons (BrdU/DCX/NeuN-positive) and increased the number of new glial cells (BrdU/GFAP-positive). These findings demonstrate that exposure to tobacco smoke diminishes neurogenesis and promotes gliogenesis in the dentate gyrus of adolescent rats. These effects may play a role in the increased risk for depression and cognitive impairment in adolescent smokers.

摘要

脑疾病和环境因素会影响海马体中的神经发生和神经胶质发生。这些研究调查了慢性暴露于烟草烟雾对青春期大鼠齿状回祖细胞增殖以及新细胞存活和表型的影响。大鼠每天暴露于烟草烟雾中 4 小时,共 14 天。为了研究细胞增殖,在外源性标记物 5-溴-2'-脱氧尿苷(BrdU,200mg/kg,ip)于第 14 天的 4 小时烟雾暴露期间的第 2 小时给予。大鼠在给予 BrdU 后 2-4 小时处死。为了研究细胞存活,在 14 天的烟雾暴露期开始前 24 小时给予相同剂量的 BrdU。这些大鼠在最后一次烟雾暴露后 24 小时处死。烟草烟雾暴露减少了齿状回中分裂祖细胞(减少 19%)和存活的新细胞(减少 20%)的数量,这些细胞用 BrdU 标记。细胞增殖的减少与细胞凋亡死亡的增加无关,如 TUNEL 分析所示。共定位研究表明,暴露于烟草烟雾减少了新不成熟神经元(BrdU/DCX 阳性)和过渡神经元(BrdU/DCX/NeuN 阳性)的数量,并增加了新胶质细胞(BrdU/GFAP 阳性)的数量。这些发现表明,暴露于烟草烟雾会减少青春期大鼠齿状回中的神经发生并促进神经胶质发生。这些影响可能在青少年吸烟者抑郁和认知障碍风险增加中发挥作用。

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