Prenatal nicotine and maternal deprivation stress de-regulate the development of CA1, CA3, and dentate gyrus neurons in hippocampus of infant rats.
Prenatal nicotine and maternal deprivation stress de-regulate the development of CA1, CA3, and dentate gyrus neurons in hippocampus of infant rats.
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DOI：
10.1371/journal.pone.0065517
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Gondré-Lewis MC
中科院分区：
文献类型：
--
作者：
Wang H;Gondré-Lewis MC
发育中的胎儿和幼儿期的不良经历对学习、情绪行为和整体认知产生深远影响。在这项研究中，我们研究了产前尼古丁暴露（NIC）、产后母亲剥夺（MD）或两者结合（NIC+MD）的影响，以确定海马神经元发育是否受到滥用药物和/或压力的影响。暴露于单独MD或NIC+MD的大鼠后代的生长受到抑制，直到断奶后。在出生后第 14 天 (P14) 幼崽的 CA1 中，MD 增加了锥体神经元，但在齿状回 (DG) 中，颗粒神经元减少。 NIC 对 CA1、CA3 或 DG 中的神经元数量没有影响。出乎意料的是，NIC 与 MD 的结合引起了 CA1 或 CA3 神经元数量的协同增加。 CA 区域的神经元密度未受治疗影响，但在 DG 中，在 NIC、MD 或 NIC+MD 暴露后，颗粒神经元的堆积密度较松散。当分析间隔颞轴时，CA1 和 CA3 中应激和药物暴露的协同作用与喙相关，而 MD 效应主要与尾神经元相关。 TUNEL 标记表明在 P14 时没有活跃的细胞凋亡，并且相对于对照组，NIC+MD 中双皮质素阳性神经元和苔藓纤维减少。还分析了尼古丁和/或母性剥夺对右海马体和左海马体的影响的偏侧性，发现其影响微不足道。我们首次报道，早期生活压力源（例如产后 MD 和产前 NIC 暴露）结合起来，可能会对 CA1 和 CA3 锥体神经元发育产生协同作用，并对发育中的 DG 神经元产生潜在的拮抗影响。这些结果表明，早期应激源可能在神经发育的关键时期以区域特异性方式调节海马谷氨酸能神经元的神经发生、凋亡或成熟。
Adverse experiences by the developing fetus and in early childhood are associated with profound effects on learning, emotional behavior, and cognition as a whole. In this study we investigated the effects of prenatal nicotine exposure (NIC), postnatal maternal deprivation (MD) or the combination of the two (NIC+MD) to determine if hippocampal neuron development is modulated by exposure to drugs of abuse and/or stress. Growth of rat offspring exposed to MD alone or NIC+MD was repressed until after weaning. In CA1 but not CA3 of postnatal day 14 (P14) pups, MD increased pyramidal neurons, however, in dentate gyrus (DG), decreased granule neurons. NIC had no effect on neuron number in CA1, CA3 or DG. Unexpectedly, NIC plus MD combined caused a synergistic increase in the number of CA1 or CA3 neurons. Neuron density in CA regions was unaffected by treatment, but in the DG, granule neurons had a looser packing density after NIC, MD or NIC+MD exposure. When septotemporal axes were analyzed, the synergism of stress and drug exposure in CA1 and CA3 was associated with rostral, whereas MD effects were predominantly associated with caudal neurons. TUNEL labeling suggests no active apoptosis at P14, and doublecortin positive neurons and mossy fibers were diminished in NIC+MD relative to controls. The laterality of the effect of nicotine and/or maternal deprivation in right versus left hippocampus was also analyzed and found to be insiginificant. We report for the first time that early life stressors such as postnatal MD and prenatal NIC exposure, when combined, may exhibit synergistic consequences for CA1 and CA3 pyramidal neuron development, and a potential antagonistic influence on developing DG neurons. These results suggest that early stressors may modulate neurogenesis, apoptosis, or maturation of glutamatergic neurons in the hippocampus in a region-specific manner during critical periods of neurodevelopment.
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影响因子：
16.2
作者：
Fanselow, Michael S.;Dong, Hong-Wei
通讯作者：
Dong, Hong-Wei
DOI：
10.1016/s0736-5748(98)00019-7
发表时间：
1998-06-01
影响因子：
1.8
作者：
Biagini, G;Pich, EM;Agnati, LF
通讯作者：
Agnati, LF
影响因子：
4.7
作者：
Dávila-García, MI;Musachio, JL;Kellar, KJ
通讯作者：
Kellar, KJ
早期压力作为酒精和药物依赖性的预测因素。
影响因子：
3.4
作者：
Enoch, Mary-Anne
通讯作者：
Enoch, Mary-Anne
影响因子：
10.6
作者：
Enoch, Mary-Anne;Hodgkinson, Colin A.;Yuan, Qiaoping;Shen, Pei-Hong;Goldman, David;Roy, Alec
通讯作者：
Roy, Alec