School of Health Sciences.
Spinal Cord and Brain Injury Research Group, Stark Neuroscience Research Institute.
Toxicol Sci. 2018 Jun 1;163(2):592-608. doi: 10.1093/toxsci/kfy062.
Adult neurogenesis takes place in the brain subventricular zone (SVZ) in the lateral walls of lateral ventricles and subgranular zone (SGZ) in the hippocampal dentate gyrus (HDG), and functions to supply newborn neurons for normal brain functionality. Subchronic Mn exposure is known to disrupt adult neurogenesis in the SVZ. This study was designed to determine whether Mn exposure disturbed neurogenesis within the adult HDG. Adult rats (10 weeks old) received a single dose of bromodeoxyuridine (BrdU) at the end of 4-week Mn exposure to label the proliferating cells. Immunostaining and cell counting data showed that BrdU(+) cells in Mn-exposed HDG were about 37% lower than that in the control (p < .05). The majority of BrdU(+) cells were identified as Sox2(+) cells. Another set of adult rats received BrdU injections for 3 consecutive days followed by 2- or 4-week Mn exposure to trace the fate of BrdU-labeled cells in the HDG. The time course studies indicated that Mn exposure significantly reduced the survival rate (54% at 2 weeks and 33% at 4 weeks), as compared with that in the control (80% at 2 weeks and 51% at 4 weeks) (p < .01). A significant time-dependent migration of newborn cells from the SGZ toward the granule cell layer was also observed in both control and Mn-exposed HDG. Triple-stained neuroblasts and mature neurons further revealed that Mn exposure significantly inhibited the differentiation of immature neuroblasts into mature neurons in the HDG. Taken together, these observations suggest that subchronic Mn exposure results in a reduced cell proliferation, diminished survival of adult-born neurons, and inhibited overall neurogenesis in the adult HDG. Impaired adult neurogenesis is likely one of the mechanisms contribute to Mn-induced Parkinsonian disorder.
成人神经发生发生在侧脑室外侧壁的脑室下区(SVZ)和海马齿状回的颗粒下区(SGZ),其功能是为正常大脑功能提供新生神经元。已知亚慢性 Mn 暴露会破坏 SVZ 中的成人神经发生。本研究旨在确定 Mn 暴露是否会干扰成年 HDG 中的神经发生。成年大鼠(10 周龄)在 4 周 Mn 暴露结束时接受单次溴脱氧尿苷(BrdU)注射,以标记增殖细胞。免疫染色和细胞计数数据显示,Mn 暴露 HDG 中的 BrdU(+)细胞比对照组低约 37%(p<0.05)。大多数 BrdU(+)细胞被鉴定为 Sox2(+)细胞。另一组成年大鼠连续 3 天接受 BrdU 注射,然后接受 2 或 4 周 Mn 暴露,以追踪 HDG 中 BrdU 标记细胞的命运。时程研究表明,与对照组(2 周时为 80%,4 周时为 51%)相比,Mn 暴露显著降低了细胞存活率(2 周时为 54%,4 周时为 33%)(p<0.01)。在对照和 Mn 暴露的 HDG 中也观察到新生细胞从 SGZ 向颗粒细胞层的显著时间依赖性迁移。三重染色的神经前体细胞和成熟神经元进一步表明,Mn 暴露显著抑制了 HDG 中未成熟神经前体细胞向成熟神经元的分化。综上所述,这些观察结果表明,亚慢性 Mn 暴露导致细胞增殖减少、成年新生神经元存活率降低以及成年 HDG 中的整体神经发生受到抑制。受损的成人神经发生可能是 Mn 诱导的帕金森病的机制之一。