Assessment of Adult Neurogenesis in Mice

Pan, Yii‐Wen; Wang, Wenbin; Xia, Zhengui

doi:10.1002/0471140856.tx1220s56

Cited by 9 publications

(11 citation statements)

References 24 publications

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“…Various extracellular and intracellular stimuli have been shown to modulate the survival, proliferation, and differentiation of adult-born cells in the hippocampus (Clelland et al ., 2009; Deng et al, 2009; Garthe et al ., 2009; Ming and Song, 2011; Pan et al, 2013b; Wang et al ., 2013). However, the effects of toxicants on adult neurogenesis are not well understood.…”

Section: Discussionmentioning

confidence: 99%

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Lead decreases cell survival, proliferation, and neuronal differentiation of primary cultured adult neural precursor cells through activation of the JNK and p38 MAP kinases

Engstrom

Wang

Xia

2015

Toxicology in Vitro

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Adult hippocampal neurogenesis is the process whereby adult neural precursor cells (aNPCs) in the subgranular zone (SGZ) of the dentate gyrus (DG) generate adult-born, functional neurons in the hippocampus. This process is modulated by various extracellular and intracellular stimuli, and the adult-born neurons have been implicated in hippocampus-dependent learning and memory. However, studies on how neurotoxic agents affect this process and the underlying mechanisms are limited. The goal of this study was to determine whether lead, a heavy metal, directly impairs critical processes in adult neurogenesis and to characterize the underlying signaling pathways using primary cultured SGZ-aNPCs isolated from adult mice. We report here that lead significantly increases apoptosis and inhibits proliferation in SGZ-aNPCs. In addition, lead significantly impairs spontaneous neuronal differentiation and maturation. Furthermore, we found that activation of the c-Jun NH2-terminal kinase (JNK) and p38 mitogen activated protein (MAP) kinase signaling pathways are important for lead cytotoxicity. Our data suggest that lead can directly act on adult neural stem cells and impair critical processes in adult hippocampal neurogenesis, which may contribute to its neurotoxicity and adverse effects on cognition in adults.

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Section: Discussionmentioning

confidence: 99%

“…The primary aNPCs were prepared as previously described (Guo et al, 2012; Pan et al, 2013) from the SGZ of the DG from 6-7 week-old male C57BL/6J mice (Taconic, Hudson, NY). The solutions and media used during the aNPC isolation were filter sterilized.…”

Section: Methodsmentioning

confidence: 99%

Lead decreases cell survival, proliferation, and neuronal differentiation of primary cultured adult neural precursor cells through activation of the JNK and p38 MAP kinases

Engstrom

Wang

Xia

2015

Toxicology in Vitro

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“…Each animal was weighed and given an initial dose of 100-mg/kg BrdU by intraperitoneal injection. Mice received four more doses of 100-mg/kg BrdU given at 2-h intervals, resulting in a cumulative dose of 500 mg/kg/day (Pan et al 2013a; Taupin 2007). …”

Section: Methodsmentioning

confidence: 99%

“…For NeuN/BrdU immunohistochemistry, animals were pre-treated with 500-mg/kg BrdU the day before exposure, exposed for 6 h, then euthanized 21 days following exposure, to label adult-born cells that are still alive. Their brains were fixed, frozen, and sectioned as described above, and stored at − 80 °C in cryoprotectant medium (Pan et al 2013a). …”

Section: Methodsmentioning

confidence: 99%

Acute exposure to diesel exhaust impairs adult neurogenesis in mice: prominence in males and protective effect of pioglitazone

et al. 2018

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Adult neurogenesis is the process by which neural stem cells give rise to new functional neurons in specific regions of the adult brain, a process that occurs throughout life. Significantly, neurodegenerative and psychiatric disorders present suppressed neurogenesis, activated microglia, and neuroinflammation. Traffic-related air pollution has been shown to adversely affect the central nervous system. As the cardinal effects of air pollution exposure are microglial activation, and ensuing oxidative stress and neuroinflammation, we investigated whether acute exposures to diesel exhaust (DE) would inhibit adult neurogenesis in mice. Mice were exposed for 6 h to DE at a PM concentration of 250-300 μg/m, followed by assessment of adult neurogenesis in the hippocampal subgranular zone (SGZ), the subventricular zone (SVZ), and olfactory bulb (OB). DE impaired cellular proliferation in the SGZ and SVZ in males, but not females. DE reduced adult neurogenesis, with male mice showing fewer new neurons in the SGZ, SVZ, and OB, and females showing fewer new neurons only in the OB. To assess whether blocking microglial activation protected against DE-induced suppression of adult hippocampal neurogenesis, male mice were pre-treated with pioglitazone (PGZ) prior to DE exposure. The effects of DE exposure on microglia, as well as neuroinflammation and oxidative stress, were reduced by PGZ. PGZ also antagonized DE-induced suppression of neurogenesis in the SGZ. These results suggest that DE exposure impairs adult neurogenesis in a sex-dependent manner, by a mechanism likely to involve microglia activation and neuroinflammation.

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“…The primary aNPCs were prepared as previously described(Guo et al, 2012; Pan et al, 2013a; Pan et al, 2013b; Pan et al, 2012) from the SVZ of the lateral ventricle from 9.5 week-old male C57BL/6J mice. The solutions and media used during the SVZ-aNPCs isolation were filter sterilized.…”

Section: Methodsmentioning

confidence: 99%

Cadmium impairs the survival and proliferation of cultured adult subventricular neural stem cells through activation of the JNK and p38 MAP kinases

2017

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Cadmium (Cd) is a heavy metal with a long biological half-life in humans and is recognized as a toxic pollutant. Cd is also a potential neurotoxicant and its exposure is associated with olfactory impairment in humans. However, the molecular and cellular mechanisms of Cd neurotoxicity are not well defined. Adult neurogenesis is a process that generates functional neurons from adult neural stem/progenitor cells (aNPCs). It occurs in specific regions of the adult brain including the subventricular zone (SVZ) along the lateral ventricles in mammals, a process that is critical for olfaction. Various external stimuli can modulate adult neurogenesis and the effect of neurotoxicants on adult neurogenesis is just beginning to be elucidated. Since Cd exposure can impair olfaction in humans, the goal of this study is to investigate the effects of Cd on SVZ adult neurogenesis and underlying mechanisms using primary cultured SVZ-aNPCs. In this study, we report that low-level Cd exposure decreases cell number, induces apoptosis, and inhibits cell proliferation in SVZ-aNPCs. Furthermore, Cd exposure significantly increases phosphorylation of c-Jun NH2-terminal kinase (JNK), and p38 MAP kinase in these cells, indicative of JNK and p38 activation. Pharmacological inhibition of JNK or p38 MAPK kinases attenuated Cd-induced cell loss and apoptosis. Cd treatment did not cause cell loss or apoptosis in SVZ-aNPCs prepared from transgenic mice null for the neural-specific JNK3 isoform. These data suggest a critical role for p38 and JNK3 MAP kinases in Cd neurotoxicity. These results are, to our knowledge, the first demonstration that Cd impairs SVZ adult neurogenesis in vitro, which may contribute to its neurotoxicity in olfaction.

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Assessment of Adult Neurogenesis in Mice

Cited by 9 publications

References 24 publications

Lead decreases cell survival, proliferation, and neuronal differentiation of primary cultured adult neural precursor cells through activation of the JNK and p38 MAP kinases

Lead decreases cell survival, proliferation, and neuronal differentiation of primary cultured adult neural precursor cells through activation of the JNK and p38 MAP kinases

Acute exposure to diesel exhaust impairs adult neurogenesis in mice: prominence in males and protective effect of pioglitazone

Cadmium impairs the survival and proliferation of cultured adult subventricular neural stem cells through activation of the JNK and p38 MAP kinases

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