Journal articles on the topic 'Meninges, neural stem cells, postnatal neurogenesis'
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1
Ban, Jelena, and Miranda Mladinic. "Spinal cord neural stem cells heterogeneity in postnatal development." STEMedicine 1, no. 1 (January 2, 2020): e19. http://dx.doi.org/10.37175/stemedicine.v1i1.19.
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Neural stem cells are capable of generating new neurons during development as well as in the adulthood and represent one of the most promising tools to replace lost or damaged neurons after injury or neurodegenerative disease. Unlike the brain, neurogenesis in the adult spinal cord is poorly explored and the comprehensive characterization of the cells that constitute stem cell neurogenic niche is still missing. Moreover, the terminology used to specify developmental and/or anatomical CNS regions, where neurogenesis in the spinal cord occurs, is not consensual and the analogy with the brain is often unclear. In this review, we will try to describe the heterogeneity of the stem cell types in the spinal cord ependymal zone, based on their origin and stem cell potential. We will also consider specific animal in vitro models that could be useful to identify “the right” stem cell candidate for cell replacement therapies.
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Kulcenty, Katarzyna Ida, Joanna Patrycja Wróblewska, and Wiktoria Maria Suchorska. "Response of neural stem cells to ionizing radiation." Letters in Oncology Science 15, no. 4 (January 7, 2019): 157–60. http://dx.doi.org/10.21641/los.15.4.115.
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Adult neurons are believed to be in a state of growth arrest. The generation of neurons is complete at the time of birth in most of the brain regions. However neurogenesis is present through life in the dentate gyrus of hippocampus and the lateral ventricles due to the presence of neural stem cells (NSC). This postnatal neurogenesis in hippocampus plays a critical role in cognitive development mainly in learning and memory functions. NSC are self-renewing, multipotent cells that generate the neurons and glia of the nervous system. Due to their high proliferation, NSC are highly sensitive to ionizing radiation. This review describes the current knowledge on impact of ionizing radiation on neural stem cells biology. Widening the knowledge of mechanisms involved in radiation-induced neurotoxicity at the level of NSC may help to overcome in the future the side effects occurring after anti-cancer therapies of the brain and help to protect and maintain neurogenesis.
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Tsupykov, O. "Neural stem cell niches in the adult mammalian brain." Cell and Organ Transplantology 3, no. 2 (November 30, 2015): 190–94. http://dx.doi.org/10.22494/cot.v3i2.13.
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Stem cells of the central nervous system have received a great deal of attention in neurobiology in the last decade. It has been shown that neurogenesis occurs in the postnatal period in specialized niches of the adult mammalian brain. The niche is a key regulator of stem cell behavior. Recent data underscore the complexity and heterogeneity of the different components of the niche, and the presence of local signaling microdomain. The review is devoted to recent views on the structural organization of neurogenic niches and regulatory factors involved at different stages of neurogenesis in the postnatal period. Understanding of stem cells behavior in the niches can serve as a basis for determination of these cells function in the adult brain.
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Nieto-González, Jose L., Leonardo Gómez-Sánchez, Fabiola Mavillard, Pedro Linares-Clemente, María C. Rivero, Marina Valenzuela-Villatoro, José L. Muñoz-Bravo, Ricardo Pardal, and Rafael Fernández-Chacón. "Loss of postnatal quiescence of neural stem cells through mTOR activation upon genetic removal of cysteine string protein-α." Proceedings of the National Academy of Sciences 116, no. 16 (March 29, 2019): 8000–8009. http://dx.doi.org/10.1073/pnas.1817183116.
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Neural stem cells continuously generate newborn neurons that integrate into and modify neural circuitry in the adult hippocampus. The molecular mechanisms that regulate or perturb neural stem cell proliferation and differentiation, however, remain poorly understood. Here, we have found that mouse hippocampal radial glia-like (RGL) neural stem cells express the synaptic cochaperone cysteine string protein-α (CSP-α). Remarkably, in CSP-α knockout mice, RGL stem cells lose quiescence postnatally and enter into a high-proliferation regime that increases the production of neural intermediate progenitor cells, thereby exhausting the hippocampal neural stem cell pool. In cell culture, stem cells in hippocampal neurospheres display alterations in proliferation for which hyperactivation of the mechanistic target of rapamycin (mTOR) signaling pathway is the primary cause of neurogenesis deregulation in the absence of CSP-α. In addition, RGL cells lose quiescence upon specific conditional targeting of CSP-α in adult neural stem cells. Our findings demonstrate an unanticipated cell-autonomic and circuit-independent disruption of postnatal neurogenesis in the absence of CSP-α and highlight a direct or indirect CSP-α/mTOR signaling interaction that may underlie molecular mechanisms of brain dysfunction and neurodegeneration.
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Li, Jingzheng, Yafang Shang, Lin Wang, Bo Zhao, Chunli Sun, Jiali Li, Siling Liu, et al. "Genome integrity and neurogenesis of postnatal hippocampal neural stem/progenitor cells require a unique regulator Filia." Science Advances 6, no. 44 (October 2020): eaba0682. http://dx.doi.org/10.1126/sciadv.aba0682.
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Endogenous DNA double-strand breaks (DSBs) formation and repair in neural stem/progenitor cells (NSPCs) play fundamental roles in neurogenesis and neurodevelopmental disorders. NSPCs exhibit heterogeneity in terms of lineage fates and neurogenesis activity. Whether NSPCs also have heterogeneous regulations on DSB formation and repair to accommodate region-specific neurogenesis has not been explored. Here, we identified a regional regulator Filia, which is predominantly expressed in mouse hippocampal NSPCs after birth and regulates DNA DSB formation and repair. On one hand, Filia protects stalling replication forks and prevents the replication stress-associated DNA DSB formation. On the other hand, Filia facilitates the homologous recombination–mediated DNA DSB repair. Consequently, Filia−/− mice had impaired hippocampal NSPC proliferation and neurogenesis and were deficient in learning, memory, and mood regulations. Thus, our study provided the first proof of concept demonstrating the region-specific regulations of DSB formation and repair in subtypes of NSPCs.
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Anesti, Maria, Stavroula Magkafa, Efstathia Prantikou, and Ilias Kazanis. "Divergence between Neuronal and Oligodendroglial Cell Fate, in Postnatal Brain Neural Stem Cells, Leads to Divergent Properties in Polymorphic In Vitro Assays." Cells 11, no. 11 (May 25, 2022): 1743. http://dx.doi.org/10.3390/cells11111743.
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Two main stem cell pools exist in the postnatal mammalian brain that, although they share some “stemness” properties, also exhibit significant differences. Multipotent neural stem cells survive within specialized microenvironments, called niches, and they are vulnerable to ageing. Oligodendroglial lineage-restricted progenitor cells are widely distributed in the brain parenchyma and are more resistant to the effects of ageing. Here, we create polymorphic neural stem cell cultures and allow cells to progress towards the neuronal and the oligodendroglial lineage. We show that the divergence of cell fate is accompanied by a divergence in the properties of progenitors, which reflects their adaptation to life in the niche or the parenchyma. Neurogenesis shows significant spatial restrictions and a dependence on laminin, a major niche component, while oligodendrogenesis shows none of these constraints. Furthermore, the blocking of integrin-β1 leads to opposing effects, reducing neurogenesis and enhancing oligodendrogenesis. Therefore, polymorphic neural stem cell assays can be used to investigate the divergence of postnatal brain stem cells and also to predict the in vivo effects of potential therapeutic molecules targeting stem and progenitor cells, as we do for the microneurotrophin BNN-20.
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Lim, Daniel A., Yin-Cheng Huang, Tomek Swigut, Anika L. Mirick, Jose Manuel Garcia-Verdugo, Joanna Wysocka, Patricia Ernst, and Arturo Alvarez-Buylla. "Chromatin remodelling factor Mll1 is essential for neurogenesis from postnatal neural stem cells." Nature 458, no. 7237 (February 11, 2009): 529–33. http://dx.doi.org/10.1038/nature07726.
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Brooks, Arrin C., and Brandon J. Henderson. "Systematic Review of Nicotine Exposure’s Effects on Neural Stem and Progenitor Cells." Brain Sciences 11, no. 2 (January 29, 2021): 172. http://dx.doi.org/10.3390/brainsci11020172.
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While various modalities of chronic nicotine use have been associated with numerous negative consequences to human health, one possible benefit of nicotine exposure has been uncovered. The discovery of an inverse correlation between smoking and Parkinson’s disease, and later Alzheimer’s disease as well, motivated investigation of nicotine as a neuroprotective agent. Some studies have demonstrated that nicotine elicits improvements in cognitive function. The hippocampus, along with the subventricular zone (SVZ), is a distinct brain region that allow for ongoing postnatal neurogenesis throughout adulthood and plays a major role in certain cognitive behaviors like learning and memory. Therefore, one hypothesis underlying nicotine-induced neuroprotection is possible effects on neural stem cells and neural precursor cells. On the other hand, nicotine withdrawal frequently leads to cognitive impairments, particularly in hippocampal-dependent behaviors, possibly suggesting an impairment of hippocampal neurogenesis with nicotine exposure. This review discusses the current body of evidence on nicotine’s effects on neural stem cells and neural progenitors. Changes in neural stem cell proliferation, survival, intracellular dynamics, and differentiation following acute and chronic nicotine exposure are examined.
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Bonfanti, Luca. "The (Real) Neurogenic/Gliogenic Potential of the Postnatal and Adult Brain Parenchyma." ISRN Neuroscience 2013 (February 6, 2013): 1–14. http://dx.doi.org/10.1155/2013/354136.
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During the last two decades basic research in neuroscience has remarkably expanded due to the discovery of neural stem cells (NSCs) and adult neurogenesis in the mammalian central nervous system (CNS). The existence of such unexpected plasticity triggered hopes for alternative approaches to brain repair, yet deeper investigation showed that constitutive mammalian neurogenesis is restricted to two small “neurogenic sites” hosting NSCs as remnants of embryonic germinal layers and subserving homeostatic roles in specific neural systems. The fact that in other classes of vertebrates adult neurogenesis is widespread in the CNS and useful for brain repair sometimes creates misunderstandings about the real reparative potential in mammals. Nevertheless, in the mammalian CNS parenchyma, which is commonly considered as “nonneurogenic,” some processes of gliogenesis and, to a lesser extent, neurogenesis also occur. This “parenchymal” cell genesis is highly heterogeneous as to the position, identity, and fate of the progenitors. In addition, even the regional outcomes are different. In this paper the heterogeneity of mammalian parenchymal neurogliogenesis will be addressed, also discussing the most common pitfalls and misunderstandings of this growing and promising research field.
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Shah, Kushani, Gwendalyn D. King, and Hao Jiang. "A chromatin modulator sustains self-renewal and enables differentiation of postnatal neural stem and progenitor cells." Journal of Molecular Cell Biology 12, no. 1 (August 23, 2019): 4–16. http://dx.doi.org/10.1093/jmcb/mjz036.
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Abstract It remains unknown whether H3K4 methylation, an epigenetic modification associated with gene activation, regulates fate determination of the postnatal neural stem and progenitor cells (NSPCs). By inactivating the Dpy30 subunit of the major H3K4 methyltransferase complexes in specific regions of mouse brain, we demonstrate a crucial role of efficient H3K4 methylation in maintaining both the self-renewal and differentiation capacity of postnatal NSPCs. Dpy30 deficiency disrupts development of hippocampus and especially the dentate gyrus and subventricular zone, the major regions for postnatal NSC activities. Dpy30 is indispensable for sustaining the self-renewal and proliferation of NSPCs in a cell-intrinsic manner and also enables the differentiation of mouse and human neural progenitor cells to neuronal and glial lineages. Dpy30 directly regulates H3K4 methylation and the induction of several genes critical in neurogenesis. These findings link a prominent epigenetic mechanism of gene expression to the fundamental properties of NSPCs and may have implications in neurodevelopmental disorders.
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Li, Yutong, Nicole Leanne Dittmann, Adrianne Eve Scovil Watson, Monique Marylin Alves de Almeida, Tim Footz, and Anastassia Voronova. "Hepatoma Derived Growth Factor Enhances Oligodendrocyte Genesis from Subventricular Zone Precursor Cells." ASN Neuro 14 (January 2022): 175909142210863. http://dx.doi.org/10.1177/17590914221086340.
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Oligodendrocytes, the myelinating cells of the central nervous system (CNS), perform vital functions in neural protection and communication, as well as cognition. Enhanced production of oligodendrocytes has been identified as a therapeutic approach for neurodegenerative and neurodevelopmental disorders. In the postnatal brain, oligodendrocytes are generated from the neural stem and precursor cells (NPCs) in the subventricular zone (SVZ) and parenchymal oligodendrocyte precursor cells (OPCs). Here, we demonstrate exogenous Hepatoma Derived Growth Factor (HDGF) enhances oligodendrocyte genesis from murine postnatal SVZ NPCs in vitro without affecting neurogenesis or astrogliogenesis. We further show that this is achieved by increasing proliferation of both NPCs and OPCs, as well as OPC differentiation into oligodendrocytes. In vivo results demonstrate that intracerebroventricular infusion of HDGF leads to increased oligodendrocyte genesis from SVZ NPCs, as well as OPC proliferation. Our results demonstrate a novel role for HDGF in regulating SVZ precursor cell proliferation and oligodendrocyte differentiation. Summary Statement Hepatoma derived growth factor (HDGF) is produced by neurons. However, its role in the central nervous system is largely unknown. We demonstrate HDGF enhances i) oligodendrocyte formation from subventricular zone neural stem cells, and ii) oligodendrocyte precursor proliferation in vitro and in vivo.
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Lopatina, Olga L., Natalia A. Malinovskaya, Yulia K. Komleva, Yana V. Gorina, Anton N. Shuvaev, Raisa Y. Olovyannikova, Olga S. Belozor, Olga A. Belova, Haruhiro Higashida, and Alla B. Salmina. "Excitation/inhibition imbalance and impaired neurogenesis in neurodevelopmental and neurodegenerative disorders." Reviews in the Neurosciences 30, no. 8 (November 26, 2019): 807–20. http://dx.doi.org/10.1515/revneuro-2019-0014.
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AbstractThe excitation/inhibition (E/I) balance controls the synaptic inputs to prevent the inappropriate responses of neurons to input strength, and is required to restore the initial pattern of network activity. Various neurotransmitters affect synaptic plasticity within neural networks via the modulation of neuronal E/I balance in the developing and adult brain. Less is known about the role of E/I balance in the control of the development of the neural stem and progenitor cells in the course of neurogenesis and gliogenesis. Recent findings suggest that neural stem and progenitor cells appear to be the target for the action of GABA within the neurogenic or oligovascular niches. The same might be true for the role of neuropeptides (i.e. oxytocin) in neurogenic niches. This review covers current understanding of the role of E/I balance in the regulation of neuroplasticity associated with social behavior in normal brain, and in neurodevelopmental and neurodegenerative diseases. Further studies are required to decipher the GABA-mediated regulation of postnatal neurogenesis and synaptic integration of newly-born neurons as a potential target for the treatment of brain diseases.
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González-Martínez, Jorge A., William E. Bingaman, Steven A. Toms, and Imad M. Najm. "Neurogenesis in the postnatal human epileptic brain." Journal of Neurosurgery 107, no. 3 (September 2007): 628–35. http://dx.doi.org/10.3171/jns-07/09/0628.
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Object The normal adult human telencephalon does not reveal evidence of spontaneous neuronal migration and differentiation despite the robust germinal capacity of the subventricular zone (SVZ) astrocyte ribbon that contains neural stem cells. This might be because it is averse to accepting new neurons into an established neuronal network, probably representing an evolutionary acquisition to prevent the formation of anomalous neuronal circuits. Some forms of epilepsy, such as malformations of cortical development, are thought to be due to abnormal corticogenesis during the embryonic and early postnatal periods. The role of postnatal architectural reorganization and possibly postnatal neurogenesis in some forms of epilepsy in humans remains unknown. In this study the authors used resected specimens of epileptic brain to determine whether neurogenesis could occur in the diseased tissue. Methods The authors studied freshly resected brain tissue obtained in 47 patients who underwent neurosurgical procedures and four autopsies. Forty-four samples were harvested in patients who underwent resection for the treatment of pharmacoresistant epilepsy. Results Using organotypic brain slice preparations cultured with 5-bromodeoxyuridine (a marker for cell proliferation), immunohistochemistry, and cell trackers, the authors demonstrate the presence of spontaneous cell proliferation, migration, and neuronal differentiation in the adult human telencephalon that starts in the SVZ and progresses to the adjacent white matter and neocortex in human neocortical pathological structures associated with epilepsy. No cell migration or neuronal differentiation was found in the control group. Conclusions The presence of spontaneous neurogenesis associated with some forms of human neocortical epilepsy may represent an erroneous and maladaptive mechanism for neuronal circuitry repair, or it may be an intrinsic part of the pathogenic process.
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Ruddy, Rebecca M., Kelsey V. Adams, and Cindi M. Morshead. "Age- and sex-dependent effects of metformin on neural precursor cells and cognitive recovery in a model of neonatal stroke." Science Advances 5, no. 9 (September 2019): eaax1912. http://dx.doi.org/10.1126/sciadv.aax1912.
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Resident neural stem and progenitor cells, collectively termed neural precursor cells (NPCs), reside in a well-defined neurogenic niche in the subventricular zone (SVZ) and contribute to ongoing postnatal neurogenesis. It is well established that the NPC niche can alter the behavior of NPCs. NPC activation is a promising therapeutic strategy for brain repair. The drug metformin has been shown to activate neural stem cells, promote differentiation, and lead to functional motor recovery in a neonatal stroke model. We demonstrate that metformin-induced NPC expansion and functional recovery is sex hormone dependent. Metformin increases the size of the NPC pool in adult females, but not males, and promotes cognitive recovery in a model of brain injury in females, but not males. Our data demonstrate that metformin has age- and sex-dependent effects on NPCs that correlate with functional recovery, which has important implications for neural repair.
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Hu, Xiaoxuan, Jing An, Qian Ge, Meiqi Sun, Zixuan Zhang, Zhenlu Cai, Ruolan Tan, Tianyou Ma, and Haixia Lu. "Maternal High-Fat Diet Reduces Type-2 Neural Stem Cells and Promotes Premature Neuronal Differentiation during Early Postnatal Development." Nutrients 14, no. 14 (July 8, 2022): 2813. http://dx.doi.org/10.3390/nu14142813.
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Maternal obesity or exposure to a high-fat diet (HFD) has an irreversible impact on the structural and functional development of offspring brains. This study aimed to investigate whether maternal HFD during pregnancy and lactation impairs dentate gyrus (DG) neurogenesis in offspring by altering neural stem cells (NSCs) behaviors. Pregnant Sprague-Dawley rats were fed a chow diet (CHD) or HFD (60% fat) during gestation and lactation. Pups were collected on postnatal day 1 (PND 1), PND 10 and PND 21. Changes in offspring body weight, brain structure and granular cell layer (GCL) thickness in the hippocampus were analyzed. Hippocampal NSCs behaviors, in terms of proliferation and differentiation, were investigated after immunohistochemical staining with Nestin, Ki67, SOX2, Doublecortin (DCX) and NeuN. Maternal HFD accelerated body weight gain and brain structural development in offspring after birth. It also reduced the number of NSCs and their proliferation, leading to a decrease in NSCs pool size. Furthermore, maternal HFD intensified NSCs depletion and promoted neuronal differentiation in the early postnatal development period. These findings suggest that maternal HFD intake significantly reduced the amount and capability of NSCs via reducing type–2 NSCs and promoting premature neuronal differentiation during postnatal hippocampal development.
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Walker, Avery S., Gwendolyn E. Goings, Yongsoo Kim, Richard J. Miller, Anjen Chenn, and Francis G. Szele. "Nestin Reporter Transgene Labels Multiple Central Nervous System Precursor Cells." Neural Plasticity 2010 (2010): 1–14. http://dx.doi.org/10.1155/2010/894374.
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Embryonic neuroepithelia and adult subventricular zone (SVZ) stem and progenitor cells express nestin. We characterized a transgenic line that expresses enhanced green fluorescent protein (eGFP) specified to neural tissue by the second intronic enhancer of the nestin promoter that had several novel features. During embryogenesis, the dorsal telencephalon contained many and the ventral telencephalon few eGFP+ cells. eGFP+ cells were found in postnatal and adult neurogenic regions. eGFP+ cells in the SVZ expressed multiple phenotype markers, glial fibrillary acidic protein, Dlx, and neuroblast-specific molecules suggesting the transgene is expressed through the lineage. eGFP+ cell numbers increased in the SVZ after cortical injury, suggesting this line will be useful in probing postinjury neurogenesis. In non-neurogenic regions, eGFP was strongly expressed in oligodendrocyte progenitors, but not in astrocytes, even when they were reactive. This eGFP+ mouse will facilitate studies of proliferative neuroepithelia and adult neurogenesis, as well as of parenchymal oligodendrocytes.
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Itokazu, Yutaka, Dongpei Li, and Robert K. Yu. "Intracerebroventricular Infusion of Gangliosides Augments the Adult Neural Stem Cell Pool in Mouse Brain." ASN Neuro 11 (January 2019): 175909141988485. http://dx.doi.org/10.1177/1759091419884859.
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We previously reported that ganglioside GD3 is the predominant species in neural stem cells (NSCs) and reduced postnatal NSC pools are observed in both the subventricular zone and dentate gyrus (DG) of GD3-synthase knockout (GD3S-KO) mouse brains. Specifically, deficiency of GD3 in GD3S-KO animals revealed a dramatic reduction in cellularity in the DG of the hippocampus of the developing mouse brain, resulting in severe behavioral deficits in these animals. To further evaluate the functional role of GD3 in postnatal brain, we performed rescue experiments by intracerebroventricular infusion of ganglioside GD3 in adult GD3S-KO animals and found that it could restore the NSC pools and enhance the NSCs for self-renewal. Furthermore, 5xFAD mouse model was utilized, and GD3 restored NSC numbers and GM1 promoted neuronal differentiation. Our results thus demonstrate that exogenously administered gangliosides are capable to restore the function of postnatal NSCs. Since ganglioside expression profiles are associated not only with normal brain development but also with pathogenic mechanisms of diseases, such as Alzheimer’s disease, we anticipate that the administration of exogenous gangliosides, such as GD3 and GM1, may represent a novel and effective strategy for promoting adult neurogenesis in damaged brain for disease treatment.
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Gao, Hui, Xuejun Cheng, Junchen Chen, Chai Ji, Hongfeng Guo, Wenzheng Qu, Xiaoxue Dong, et al. "Fto-modulated lipid niche regulates adult neurogenesis through modulating adenosine metabolism." Human Molecular Genetics 29, no. 16 (August 7, 2020): 2775–87. http://dx.doi.org/10.1093/hmg/ddaa171.
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Abstract Adult neurogenesis is regulated by diverse factors including the local environment, i.e. the neurogenic niche. However, whether the lipid in the brain regulates adult neurogenesis and related mechanisms remains largely unknown. In the present study, we found that lipid accumulates in the brain during postnatal neuronal development. Conditional knockout of Fto (cKO) in lipid not only reduced the level of lipid in the brain but also impaired the learning and memory of mice. In addition, Fto deficiency in lipid did not affect the proliferation of adult neural stem cells (aNSCs), but it did inhibit adult neurogenesis by inducing cell apoptosis. Mechanistically, specific deleting Fto in lipid altered gene expression and increased adenosine secretion of adipocytes. The treatment of adenosine promoted the apoptosis of newborn neurons. As a whole, these results reveal the important function of the lipid niche and its associated mechanism in regulating adult neurogenesis.
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Vancamp, Pieter, Barbara Demeneix, and Sylvie Remaud. "Postnatal Hypothyroidism Permanently Disrupts Neural Stem Cell Fate in the Murine Subventricular Zone." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A977. http://dx.doi.org/10.1210/jendso/bvab048.1997.
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Abstract The subventricular zone (SVZ) of the adult mammalian brain harbors neural stem cells (NSCs) that generate neurons and oligodendrocytes throughout life. Single-cell RNA-Seq analysis on mouse SVZ-NSCs isolated at different developmental stages established they gradually acquire their adult neurogliogenic identity between postnatal day (P) 7 and 20. However, the factors governing this transition remain elusive. As a key factor driving transcriptional responses during brain development, as well as NSC lineage commitment in the adult SVZ, we hypothesized that thyroid hormone (TH) could fulfil this role. TH serum levels rise postnatally and peak around P15. Re-analysis of single-cell data from the P2 and P20 SVZ revealed a dynamically increased expression of the TH transporters Mct8 and Oatp1c1, as well as the TH-(in)activating deiodinases Dio2 and Dio3 in NSCs, signs that local TH action is promoted. Immunostainings showed a concomitant burst in SVZ-neurogenesis between P4 and P21. Then, to study what occurs if TH synthesis is blocked, we fed dams a 0.15% propylthiouracil-enriched diet from embryonic day 15 to P21. Postnatal hypothyroidism decreased PH3-positive mitotic cell numbers at P4 and P21, whereas increased Sox2 expression coincided with a larger proportion SOX2-positive SVZ-NSCs and progenitors. In the dorsal SVZ, the main site of neurogliogenesis, less neuroblasts were detected at P21, while numbers of OLIG2-positive oligodendroglia precursors did not change significantly. Next, we prepared in vitro neurospheres from dissected SVZs of control and PTU-treated mice, and allowed them differentiate with or without exogenous T3. The neuro/glia balance in neurosphere cultures prepared from P4 animals of either condition did not change when T3 was added, suggesting perinatal NSCs are irresponsive to TH. The balance did change in T3-treated neurospheres prepared from control P21 animals, however, not in those from P21 PTU-exposed mice, suggesting hypothyroid NSCs are irresponsive to T3. Lastly, we examined 3-month-old mice that regained a normal diet following developmental PTU exposure. Fewer oligodendroglia precursors in the SVZ resulted in a lasting altered neuro/glia output. A reduced ability to remember earlier-presented odors indicates impaired olfaction, a behavior strongly depending on SVZ-neurogenesis. Taken together the data indicate that developmental hypothyroidism affects postnatal SVZ organization and permanently alters NSC lineage commitment. Our study allows to determine relevant new read-outs to identify adverse outcome events on brain development and will permit comparison with events following exposure to endocrine disruptors.
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Martínez-Herrero, Sonia, Ignacio M. Larráyoz, Laura Ochoa-Callejero, Josune García-Sanmartín, and Alfredo Martínez. "Adrenomedullin as a Growth and Cell Fate Regulatory Factor for Adult Neural Stem Cells." Stem Cells International 2012 (2012): 1–18. http://dx.doi.org/10.1155/2012/804717.
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The use of stem cells as a strategy for tissue repair and regeneration is one of the biomedical research areas that has attracted more interest in the past few years. Despite the classic belief that the central nervous system (CNS) was immutable, now it is well known that cell turnover occurs in the mature CNS. Postnatal neurogenesis is subjected to tight regulation by many growth factors, cell signals, and transcription factors. An emerging molecule involved in this process is adrenomedullin (AM). AM, a 52-amino acid peptide which exerts a plethora of physiological functions, acts as a growth and cell fate regulatory factor for adult neural stem and progenitor cells. AM regulates the proliferation rate and the differentiation into neurons, astrocytes, and oligodendrocytes of stem/progenitor cells, probably through the PI3K/Akt pathway. The active peptides derived from the AM gene are able to regulate the cytoskeleton dynamics, which is extremely important for mature neural cell morphogenesis. In addition, a defective cytoskeleton may impair cell cycle and migration, so AM may contribute to neural stem cell growth regulation by allowing cells to pass through mitosis. Regulation of AM levels may contribute to program stem cells for their use in medical therapies.
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Boström, Martina, Marie Kalm, Niklas Karlsson, Nina Hellström Erkenstam, and Klas Blomgren. "Irradiation to the Young Mouse Brain Caused Long-Term, Progressive Depletion of Neurogenesis but did not Disrupt the Neurovascular Niche." Journal of Cerebral Blood Flow & Metabolism 33, no. 6 (March 13, 2013): 935–43. http://dx.doi.org/10.1038/jcbfm.2013.34.
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We investigated the effects of ionizing radiation on microvessel structure and complexity in the hippocampus. We also assessed neurogenesis and the neurovascular niche. Postnatal day 14 male C57BL/6 mice received a single dose of 8 Gy to the whole brain and were killed 6 hours, 1 week, 7 weeks, or 1 year later. Irradiation decreased the total number of microvessels and branching points from 1 week onwards and decreased the total microvessel area 1 and 7 weeks after irradiation. After an initial increase in vascular parameter densities, concomitant with reduced growth of the hippocampus, the densities normalized with time, presumably adapting to the needs of the surrounding nonvascular tissue. Irradiation decreased the number of neural stem and progenitor cells in the hippocampus. The relative loss increased with time, resulting in almost completely ablated neurogenesis (DCX+ cells) 1 year after irradiation (77% decreased 1 week, 86% decreased 7 weeks, and 98% decreased 1 year after irradiation compared with controls). After irradiation, the distance between undifferentiated stem cells and microvessels was unaffected, and very few dying endothelial cells were detected. Taken together, these results indicate that the vasculature adjusts to the surrounding neural and glial tissue after irradiation, not vice-versa.
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Khilazheva, E. D., A. V. Morgun, E. B. Boytsova, A. I. Mosiagina, A. N. Shuvaev, N. A. Malinovskaya, Yu A. Uspenskaya, E. A. Pozhilenkova, and A. B. Salmina. "Features of the in vitro expression profile of hippocampal neurogenic niche cells during optogenetic stimulation." Biomeditsinskaya Khimiya 67, no. 1 (January 2021): 34–41. http://dx.doi.org/10.18097/pbmc20216701034.
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In the central nervous system of mammals, there are specialized areas in which neurogenesis — neurogenic niches — is observed in the postnatal period. It is believed that astrocytes in the composition of neurogenic niches play a significant role in the regulation of neurogenesis, and therefore they are considered as a promising “target” for the possible control of neurogenesis, including the use of optogenetics. In the framework of this work, we formed an in vitro model of a neurogenic niche, consisting of cerebral endothelial cells, astrocytes and neurospheres. Astrocytes in the neurogenic niche model expressed canalorodopsin ChR2 and underwent photoactivation. The effect of photoactivated astrocytes on the expression profile of neurogenic niche cells was evaluated using immunocytochemical analysis methods. It was found that intact astrocytes in the composition of the neurogenic niche contribute to neuronal differentiation of stem cells, as well as the activation of astroglia expressing photosensitive proteins, changes the expression of molecules characterized by intercellular interactions of pools of resting and proliferating cells in the composition of the neurogenic niche with the participation of NAD+ (Cx43, CD38, CD157), lactate (MCT1). In particular, the registered changes reflect a violation of the paracrine intercellular interactions of two subpopulations of cells, one of which acts as a source of NAD+, and the second as a consumer of NAD+ to ensure the processes of intracellular signal transduction; a change in the mechanisms of lactate transport due to aberrant expression of the lactate transporter MCT1 in cells forming a pool of cells developing along the neuronal path of differentiation. In general, with photostimulation of niche astrocytes, the total proliferative activity increases mainly due to neural progenitor cells, but not neural stem cells. Thus, optogenetic activation of astrocytes can become a promising tool for controlling the activity of neurogenesis processes and the formation of a local proneurogenic microenvironment in an in vitro model of a neurogenic niche.
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Embalabala, Rebecca J., Asa A. Brockman, Amanda R. Jurewicz, Jennifer A. Kong, Kaitlyn Ryan, Cristina D. Guinto, Arturo Álvarez-Buylla, Chin Chiang, and Rebecca A. Ihrie. "GLI3 Is Required for OLIG2+ Progeny Production in Adult Dorsal Neural Stem Cells." Cells 11, no. 2 (January 10, 2022): 218. http://dx.doi.org/10.3390/cells11020218.
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The ventricular–subventricular zone (V-SVZ) is a postnatal germinal niche. It holds a large population of neural stem cells (NSCs) that generate neurons and oligodendrocytes for the olfactory bulb and (primarily) the corpus callosum, respectively. These NSCs are heterogeneous and generate different types of neurons depending on their location. Positional identity among NSCs is thought to be controlled in part by intrinsic pathways. However, extrinsic cell signaling through the secreted ligand Sonic hedgehog (Shh) is essential for neurogenesis in both the dorsal and ventral V-SVZ. Here we used a genetic approach to investigate the role of the transcription factors GLI2 and GLI3 in the proliferation and cell fate of dorsal and ventral V-SVZ NSCs. We find that while GLI3 is expressed in stem cell cultures from both dorsal and ventral V-SVZ, the repressor form of GLI3 is more abundant in dorsal V-SVZ. Despite this high dorsal expression and the requirement for other Shh pathway members, GLI3 loss affects the generation of ventrally-, but not dorsally-derived olfactory interneurons in vivo and does not affect trilineage differentiation in vitro. However, loss of GLI3 in the adult dorsal V-SVZ in vivo results in decreased numbers of OLIG2-expressing progeny, indicating a role in gliogenesis.
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Tanaka, Takeshi, Hajime Abe, Masayuki Kimura, Nobuhiko Onda, Sayaka Mizukami, Toshinori Yoshida, and Makoto Shibutani. "Developmental exposure to T-2 toxin reversibly affects postnatal hippocampal neurogenesis and reduces neural stem cells and progenitor cells in mice." Archives of Toxicology 90, no. 8 (August 28, 2015): 2009–24. http://dx.doi.org/10.1007/s00204-015-1588-4.
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Ke, Yuehai, Eric E. Zhang, Kazuki Hagihara, Dongmei Wu, Yuhong Pang, Rüdiger Klein, Tom Curran, Barbara Ranscht, and Gen-Sheng Feng. "Deletion of Shp2 in the Brain Leads to Defective Proliferation and Differentiation in Neural Stem Cells and Early Postnatal Lethality." Molecular and Cellular Biology 27, no. 19 (July 23, 2007): 6706–17. http://dx.doi.org/10.1128/mcb.01225-07.
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ABSTRACT The intracellular signaling controlling neural stem/progenitor cell (NSC) self-renewal and neuronal/glial differentiation is not fully understood. We show here that Shp2, an introcellular tyrosine phosphatase with two SH2 domains, plays a critical role in NSC activities. Conditional deletion of Shp2 in neural progenitor cells mediated by Nestin-Cre resulted in early postnatal lethality, impaired corticogenesis, and reduced proliferation of progenitor cells in the ventricular zone. In vitro analyses suggest that Shp2 mediates basic fibroblast growth factor signals in stimulating self-renewing proliferation of NSCs, partly through control of Bmi-1 expression. Furthermore, Shp2 regulates cell fate decisions, by promoting neurogenesis while suppressing astrogliogenesis, through reciprocal regulation of the Erk and Stat3 signaling pathways. Together, these results identify Shp2 as a critical signaling molecule in coordinated regulation of progenitor cell proliferation and neuronal/astroglial cell differentiation.
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Wang, Chenran, Syn Yeo, Michael A. Haas, and Jun-Lin Guan. "Autophagy gene FIP200 in neural progenitors non–cell autonomously controls differentiation by regulating microglia." Journal of Cell Biology 216, no. 8 (June 20, 2017): 2581–96. http://dx.doi.org/10.1083/jcb.201609093.
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Recent studies have shown important roles for autophagy genes in the regulation of different tissue stem cells, including neural stem/progenitor cells (NSCs). However, little is known about whether autophagy can regulate NSCs through cell-extrinsic mechanisms. Here, we show that deletion of an essential autophagy gene, FIP200, in NSCs increased expression of Ccl5 and Cxcl10 in a p53-independent manner, mediating increased infiltration of microglia into the subventricular zone of both FIP200hGFAP conditional knockout (cKO) and FIP200;p53hGFAP 2cKO mice. The microglia exhibited an activated M1 phenotype consistent with their potential to inhibit differentiation of FIP200-null NSCs. Blocking either microglia infiltration or activation rescued the deficient differentiation of FIP200-null NSCs from FIP200;p53hGFAP 2cKO mice. Lastly, we showed that increased chemokine expression in FIP200-null NSCs was induced by abnormal p62 aggregate formation and activation of NF-κB signaling. Our results suggest that autophagy plays a crucial role in regulating neurogenesis and restricting local immune response in postnatal NSCs through non–cell autonomous mechanisms.
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Wang, Jing, Allison Cheng, Chandramohan Wakade, and Robert K. Yu. "Ganglioside GD3 Is Required for Neurogenesis and Long-Term Maintenance of Neural Stem Cells in the Postnatal Mouse Brain." Journal of Neuroscience 34, no. 41 (October 8, 2014): 13790–800. http://dx.doi.org/10.1523/jneurosci.2275-14.2014.
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Wang, Hong, Zhao-Wu Ma, Feng-Ming Ho, Gautam Sethi, and Feng Ru Tang. "Dual Effects of miR-181b-2-3p/SOX21 Interaction on Microglia and Neural Stem Cells after Gamma Irradiation." Cells 12, no. 4 (February 17, 2023): 649. http://dx.doi.org/10.3390/cells12040649.
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Ionizing radiation induces brain inflammation and the impairment of neurogenesis by activating microglia and inducing apoptosis in neurogenic zones. However, the causal relationship between microglial activation and the impairment of neurogenesis as well as the relevant molecular mechanisms involved in microRNA (miR) remain unknown. In the present study, we employed immunohistochemistry and real-time RT-PCR to study the microglial activation and miRNA expression in mouse brains. Real-time RT-PCR, western blot, ELISA, cell proliferation and cytotoxicity assay were used in BV2 and mouse neural stem cells (NSCs). In the mouse model, we found the acute activation of microglia at 1 day and an increased number of microglial cells at 1, 7 and 120 days after irradiation at postnatal day 3 (P3), day 10 (P10) and day 21 (P21), respectively. In cell models, the activation of BV2, a type of microglial cell line, was observed after gamma irradiation. Real-time RT-PCR analysis revealed a deceased expression of miR-181b-2-3p and an increased expression of its target SRY-related high-mobility group box transcription factor 21 (SOX21) in a dose- and time-dependent fashion. The results of the luciferase reporter assay confirmed that SOX21 was the target of miR-181b-2-3p. Furthermore, SOX21 knockdown by siRNA inhibited the activation of microglia, thereby suggesting that the direct interaction of 181b-2-3p with SOX21 might be involved in radiation-induced microglial activation and proliferation. Interestingly, the gamma irradiation of NSCs increased miR-181b-2-3p expression but decreased SOX21 mRNA, which was the opposite of irradiation-induced expression in BV2 cells. As irradiation reduced the viability and proliferation of NSCs, whereas the overexpression of SOX21 restored the impaired cell viability and promoted the proliferation of NSCs, the findings suggest that the radiation-induced interaction of miR-181b-2-3p with SOX21 may play dual roles in microglia and NSCs, respectively, leading to the impairment of brain neurogenesis.
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Sui, B., C. Chen, X. Kou, B. Li, K. Xuan, S. Shi, and Y. Jin. "Pulp Stem Cell–Mediated Functional Pulp Regeneration." Journal of Dental Research 98, no. 1 (October 29, 2018): 27–35. http://dx.doi.org/10.1177/0022034518808754.
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The preservation of vital dental pulp with vasculature and nerve components remains one of the most significant challenges in modern dentistry. Due to the immense potential for neurovascularization, mesenchymal stem cell (MSC) transplantation has shown emerging promise in regenerative medicine and dental translational practice. Actually, pulp mesenchymal stem cells, including postnatal dental pulp stem cells (from permanent teeth) and stem cells from human exfoliated deciduous teeth, possess unique properties based on their origins from neural crest or glial cells. Furthermore, they reside in a neurovascular niche and have the potential for neurogenesis, angiogenesis, and neurovascular inductive activity. According to current pulp regeneration strategies, pulp stem cell–mediated approaches to regeneration have demonstrated convincing evidence that they can rebuild the complex histologic structure of native pulp in situ with highly organized physiologic patterns or even achieve de novo regeneration of complete dental pulp tissues. More importantly, recent clinical studies emphasized in situ neurovascularization outcomes in successful regeneration of vitalized pulp via pulp stem cell transplantation. In this review, we summarize recent breakthroughs in pulp stem cell–mediated pulp regeneration, emphasizing the crucial achievement of neurovascularization. This functional pulp regeneration represents an innovative and promising approach for future regenerative endodontics.
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Zhu, Changlian, Jianfeng Gao, Niklas Karlsson, Qian Li, Yu Zhang, Zhiheng Huang, Hongfu Li, H. Georg Kuhn, and Klas Blomgren. "Isoflurane Anesthesia Induced Persistent, Progressive Memory Impairment, Caused a Loss of Neural Stem Cells, and Reduced Neurogenesis in Young, but Not Adult, Rodents." Journal of Cerebral Blood Flow & Metabolism 30, no. 5 (January 13, 2010): 1017–30. http://dx.doi.org/10.1038/jcbfm.2009.274.
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Isoflurane and related anesthetics are widely used to anesthetize children, ranging from premature babies to adolescents. Concerns have been raised about the safety of these anesthetics in pediatric patients, particularly regarding possible negative effects on cognition. The purpose of this study was to investigate the effects of repeated isoflurane exposure of juvenile and mature animals on cognition and neurogenesis. Postnatal day 14 (P14) rats and mice, as well as adult (P60) rats, were anesthetized with isoflurane for 35 mins daily for four successive days. Object recognition, place learning and reversal learning as well as cell death and cytogenesis were evaluated. Object recognition and reversal learning were significantly impaired in isoflurane-treated young rats and mice, whereas adult animals were unaffected, and these deficits became more pronounced as the animals grew older. The memory deficit was paralleled by a decrease in the hippocampal stem cell pool and persistently reduced neurogenesis, subsequently causing a reduction in the number of dentate gyrus granule cell neurons in isoflurane-treated rats. There were no signs of increased cell death of progenitors or neurons in the hippocampus. These findings show a previously unknown mechanism of neurotoxicity, causing cognitive deficits in a clearly age-dependent manner.
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Wang, Xinyan, Wen Li, Zhenshu Li, Yue Ma, Jing Yan, John X. Wilson, and Guowei Huang. "Maternal Folic Acid Supplementation During Pregnancy Promotes Neurogenesis and Synaptogenesis in Neonatal Rat Offspring." Cerebral Cortex 29, no. 8 (August 23, 2018): 3390–97. http://dx.doi.org/10.1093/cercor/bhy207.
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Abstract Maternal folic acid supplementation during pregnancy is associated with improved cognitive performances in offspring. However, the effect of supplementation on offspring’s neurogenesis and synaptogenesis is unknown, and whether supplementation should be continued throughout pregnancy is controversial. In present study, 3 groups of female rats were fed a folate-normal diet, folate-deficient diet, or folate-supplemented diet from 1 week before mating until the end of pregnancy. A fourth group fed folate-normal diet from 1 week before mating until mating, then fed folate-supplemented diet for 10 consecutive days, then fed folate-normal diet until the end of pregnancy. Offspring were sacrificed on postnatal day 0 for measurement of neurogenesis and synaptogenesis by immunofluorescence and western blot. Additionally neural stem cells (NSCs) were cultured from offspring’s hippocampus for immunocytochemical measurement of their rates of proliferation and neuronal differentiation. The results demonstrated that maternal folic acid supplementation stimulated hippocampal neurogenesis by increasing proliferation and neuronal differentiation of NSCs, and also enhanced synaptogenesis in cerebral cortex of neonatal offspring. Hippocampal neurogenesis was stimulated more when supplementation was continued throughout pregnancy instead of being limited to the periconceptional period. In conclusion, maternal folic acid supplementation, especially if continued throughout pregnancy, improves neurogenesis and synaptogenesis in neonatal offspring.
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Sall, Jeffrey W., Greg Stratmann, Jason Leong, Elliott Woodward, and Philip E. Bickler. "Propofol at Clinically Relevant Concentrations Increases Neuronal Differentiation But Is Not Toxic to Hippocampal Neural Precursor Cells In Vitro." Anesthesiology 117, no. 5 (November 1, 2012): 1080–90. http://dx.doi.org/10.1097/aln.0b013e31826f8d86.
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Background Propofol in the early postnatal period has been shown to cause brain cell death. One proposed mechanism for cognitive dysfunction after anesthesia is alteration of neural stem cell function and neurogenesis. We examined the effect of propofol on neural precursor or stem cells (NPCs) grown in vitro. Methods Hippocampal-derived NPCs from postnatal day 2 rats were exposed to propofol or Diprivan. NPCs were then analyzed for bromodeoxyuridine incorporation to measure proliferation. Cell death was measured by lactate dehydrogenase release. Immunocytochemistry was used to evaluate the expression of neuronal and glial markers in differentiating NPCs exposed to propofol. Results Propofol dose dependently increases the release of lactate dehydrogenase from NPCs under both proliferating and differentiating conditions at supraclinical concentrations (more than 7.1 µM). Both Diprivan and propofol had the same effect on NPCs. Propofol-mediated release of lactate dehydrogenase is not inhibited by blocking the γ-aminobutyric acid type A receptor or extracellular calcium influx and is not mediated by caspase-3/7. Direct γ-aminobutyric acid type A receptor activation did not have the same effect. In differentiating NPCs, 6 h of propofol at 2.1 µM increased the number neurons but not glial cells 4 days later. Increased neuronal differentiation was not blocked by bicuculline. Conclusions Only supraclinical concentrations of propofol or Diprivan kill NPCs in culture by a non-γ-aminobutyric acid type A, noncaspase-3 mechanism. Clinically relevant doses of propofol increase neuronal fate choice by a non-γ-aminobutyric acid type A mechanism.
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Wicki-Stordeur, Leigh E., and Leigh Anne Swayne. "Large Pore Ion and Metabolite-Permeable Channel Regulation of Postnatal Ventricular Zone Neural Stem and Progenitor Cells: Interplay between Aquaporins, Connexins, and Pannexins?" Stem Cells International 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/454180.
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The birth of new neurons from unspecialized neural stem and progenitor cells surrounding the lateral ventricles occurs throughout postnatal life. This process, termed neurogenesis, is complex and multistepped, encompassing several types of cellular behaviours, such as proliferation, differentiation, and migration. These behaviours are influenced by numerous factors present in the unique, permissive microenvironment. A major cellular mechanism for sensing the plethora of environmental cues directing this process is the presence of different channel forming proteins spanning the plasma membrane. So-called large pore membrane channels, which are selective for the passage of specific types of small molecules and ions, are emerging as an important subgroup of channel proteins. Here, we focus on the roles of three such large pore channels, aquaporin 4, connexin 43, and pannexin 1. We highlight both their independent functions as well as the accumulating evidence for crosstalk between them.
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Płatek, Rafał, Piotr Rogujski, Jarosław Mazuryk, Marta B. Wiśniewska, Leszek Kaczmarek, and Artur Czupryn. "Impaired Generation of Transit-Amplifying Progenitors in the Adult Subventricular Zone of Cyclin D2 Knockout Mice." Cells 11, no. 1 (January 1, 2022): 135. http://dx.doi.org/10.3390/cells11010135.
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In the adult brain, new neurons are constitutively derived from postnatal neural stem cells/progenitors located in two neurogenic regions: the subventricular zone (SVZ) of the lateral ventricles (migrating and differentiating into different subtypes of the inhibitory interneurons of the olfactory bulbs), and the subgranular layer of the hippocampal dentate gyrus. Cyclin D2 knockout (cD2-KO) mice exhibit reduced numbers of new hippocampal neurons; however, the proliferation deficiency and the dysregulation of adult neurogenesis in the SVZ required further investigation. In this report, we characterized the differentiation potential of each subpopulation of the SVZ neural precursors in cD2-KO mice. The number of newly generated cells in the SVZs was significantly decreased in cD2-KO mice compared to wild type mice (WT), and was not accompanied by elevated levels of apoptosis. Although the number of B1-type quiescent precursors (B1q) and the overall B1-type activated precursors (B1a) were not affected in the SVZ neurogenic niche, the number of transit-amplifying progenitors (TaPs) was significantly reduced. Additionally, the subpopulations of calbindin D28k and calretinin interneurons were diminished in the olfactory bulbs of cD2-KO mice. Our results suggest that cyclin D2 might be critical for the proliferation of neural precursors and progenitors in the SVZ—the transition of B1a into TaPs and, thereafter, the production of newly generated interneurons in the olfactory bulbs. Untangling regulators that functionally modulate adult neurogenesis provides a basis for the development of regenerative therapies for injuries and neurodegenerative diseases.
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Jung, Da Hee, Malk Eun Pak, Hong Ju Lee, Sung Min Ahn, Young Ju Yun, Yong-Il Shin, Hwa Kyoung Shin, Seo-Yeon Lee, and Byung Tae Choi. "Electroacupuncture on the Scalp over the Motor Cortex Ameliorates Behavioral Deficits Following Neonatal Hypoxia-Ischemia in Rats via the Activation of Neural Stem Cells." Life 10, no. 10 (October 14, 2020): 240. http://dx.doi.org/10.3390/life10100240.
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Electroacupuncture (EA) therapy via alternating current stimulation on the scalp over the motor cortex is used for the treatment of brain disorders. Perinatal hypoxia-ischemia (HI), a brain injury in newborns, leads to long-term neurologic complications. Here, we investigated whether EA could promote functional improvements and neurogenesis in a neonatal HI rat model. A neonatal HI rat model was induced by permanent ligation of the left carotid artery in postnatal day 7 pups. EA for neonatal HI rats was performed at 2 Hz (1, 3, or 5 mA; 20 min) from 4–6 weeks after birth. HI rats undergoing EA had improved motor and memory function, with the greatest improvement after 3 mA EA. The corpus callosum was significantly thicker and showed a significant increase in proliferating astrocytes in the 3 mA EA group. We observed proliferating cells and a greater number of newly developed neurons and astrocytes in the subventricular zone and dentate gyrus of the 3 mA EA group than in those of the HI group. These results suggest that EA promotes functional improvements following neonatal HI assault via the proliferation and differentiation of neural stem cells. This effect was the strongest after 3 mA EA, suggesting that this is the optimal treatment dose.
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Sánchez-Huerta, Karla, Rosaura Debbie Saldaña-Salinas, Pablo Edson Bustamante-Nieves, Adriana Jiménez, Alejandro Corzo-Cruz, Marina Martínez-Vargas, Rosalinda Guevara-Guzmán, Iván Velasco, and Enrique Estudillo. "Sucrose Consumption during Late Adolescence Impairs Adult Neurogenesis of the Ventral Dentate Gyrus without Inducing an Anxiety-like Behavior." International Journal of Molecular Sciences 23, no. 22 (November 16, 2022): 14176. http://dx.doi.org/10.3390/ijms232214176.
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Sucrose consumption impairs behavioral and cognitive functions that correlate with decreased neurogenesis in animal models. When consumed during early adolescence, this disaccharide promotes anxious and depressive behaviors, along with a reduction in the generation of new neurons in the dentate gyrus of the hippocampus. Data concerning sucrose consumption during late adolescence are lacking, and the effect of sucrose intake on the ventral dentate gyrus of the hippocampus (which modulates anxiety and depression) remains elusive. Here, we tested whether sucrose intake during late adolescence causes anxiety or impaired neurogenesis in the ventral dentate gyrus. Rats did not display anxiety-like behaviors neither at the light–dark box test nor at the open field exploration. However, there was a significant increase in proliferative cells in the subgranular zone of the ventral dentate gyrus in rats exposed to sucrose (p < 0.05). This increased proliferation corresponded to neural stem cells (Radial Type 1 cells) in the group exposed to sucrose until adulthood but was not present in rats exposed to sucrose only during late adolescence. Remarkably, the phosphorylation of ERK1/2 kinases was increased in the hippocampi of rats exposed to sucrose only during late adolescence, suggesting that the increased proliferation in this group could be mediated by the MAPK pathway. On the other hand, although no differences were found in the number of immature granular neurons, we observed more immature granular neurons with impaired dendritic orientation in both groups exposed to sucrose. Finally, GAD65/67 and BCL2 levels did not change between groups, suggesting an unaltered hippocampal GABAergic system and similar apoptosis, respectively. This information provides the first piece of evidence of how sucrose intake, starting in late adolescence, impacts ventral dentate gyrus neurogenesis and contributes to a better understanding of the effects of this carbohydrate on the brain at postnatal stages.
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Huang, He, Lu Liu, Bing Li, Pan-Pan Zhao, Chun-Mei Xu, Yang-Zi Zhu, Cheng-Hua Zhou, and Yu-Qing Wu. "Ketamine Interferes with the Proliferation and Differentiation of Neural Stem Cells in the Subventricular Zone of Neonatal Rats." Cellular Physiology and Biochemistry 35, no. 1 (2015): 315–25. http://dx.doi.org/10.1159/000369698.
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Background: Previous studies have shown ketamine can alter the proliferation and differentiation of neural stem cells (NSCs) in vitro. However, these effects have not been entirely clarified in vivo in the subventricular zone (SVZ) of neonatal rats. The present study was designed to investigate the effects of ketamine on the proliferation and differentiation of NSCs in the SVZ of neonatal rats in vivo. Methods: Postnatal day 7 (PND-7) male Sprague-Dawley rats were administered four injections of 40 mg/kg ketamine at 1-h intervals, and then 5-bromodeoxyuridine (BrdU) was injected intraperitoneally at PND-7, 9 and 13. NSC proliferation was assessed with Nestin/BrdU double-labeling immunostaining. Neuronal and astrocytic differentiation was evaluated with β-tubulin III/BrdU and GFAP/BrdU double-labeling immunostaining, respectively. The expressions of nestin, β-tubulin III and GFAP were measured using Western blot analysis. The apoptosis of NSCs and astrocytes in the SVZ of neonatal rats was evaluated using nestin/caspase-3 and GFAP/caspase-3 double-labeling immunostaining. Results: Neonatal ketamine exposure significantly reduced the number of nestin/BrdU and GFAP/BrdU double-positive cells in the SVZ. Meanwhile, the expressions of nestin and GFAP in the SVZ from the ketamine group were significantly decreased compared those in the control group. Still, no double-positive cells for nestin/caspase-3 and GFAP/caspase-3 were found after ketamine exposure. In addition, the neuronal differentiation of NSCs in the SVZ was markedly promoted by ketamine with an increased number of β-tubulin III/BrdU double-positive cells and enhanced expression of β-tubulin III. These effects of ketamine on the NSCs in the SVZ often lasted at least 1 week after ketamine anesthesia. Conclusion: In the present study, it was demonstrated that ketamine could alter neurogenesis by inhibiting the proliferation of NSCs, suppressing their differentiation into astrocytes and promoting the neuronal differentiation of the NSCs in the SVZ of neonatal rats during a critical period of their neurodevelopment.
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Müller, Dieter, Balanes Hida, Gabriela Guidone, Robert C. Speth, Tatyana V. Michurina, Grigori Enikolopov, and Ralf Middendorff. "Expression of Guanylyl Cyclase (GC)-A and GC-B during Brain Development: Evidence for a Role of GC-B in Perinatal Neurogenesis." Endocrinology 150, no. 12 (October 16, 2009): 5520–29. http://dx.doi.org/10.1210/en.2009-0490.
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Abstract Atrial (ANP) and C-type (CNP) natriuretic peptide generate physiological effects via selective activation of two closely related membrane receptors with guanylyl cyclase (GC) activity, known as GC-A and GC-B. As yet, however, the discrete roles for ANP/GC-A vs. CNP/GC-B signaling in many mammalian tissues are still poorly understood. We here used receptor affinity labeling and GC assays to characterize comparatively GC-A/GC-B expression and functional activity during rat brain development. The study revealed that GC-B predominates in the developing and GC-A in the adult brain, with regional differences each between cerebral cortex, cerebellum, and brain stem. Whereas GC-A levels nearly continuously increase between embryonal d 18 and adult, GC-B expression in brain is highest and widely distributed around postnatal d 1. The striking perinatal GC-B peak coincides with elevated expression of nestin, a marker protein for neural stem/progenitor cells. Immunohistochemical investigations revealed a cell body-restricted subcellular localization of GC-B and perinatal abundance of GC-B-expressing cells in regions high in nestin-expressing cells. However, and supported by examination of nestin-GFP transgenic mice, GC-B and nestin are not coexpressed in the same cells. Rather, GC-B+ cells are distinguished by expression of NeuN, an early marker of differentiating neurons. These findings suggest that GC-B+ cells represent neuronal fate-specific progeny of nestin+ progenitors and raise the attention to specific and pronounced activities of CNP/GC-B signaling during perinatal brain maturation. The absence of this activity may cause the neurological disorders observed in GC-B-deficient mice.
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Wang, Ning, Yang Lu, Kui Wang, Wei-song Li, Pan Lu, Shan Lei, Rong Li, et al. "Simvastatin Attenuates Neurogenetic Damage and Improves Neurocongnitive Deficits Induced by Isoflurane in Neonatal Rats." Cellular Physiology and Biochemistry 46, no. 2 (2018): 618–32. http://dx.doi.org/10.1159/000488630.
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Background/Aims: Isoflurane inhibited neurogenesis and induced subsequent neurocognitive deficits in developing brain. Simvastatin exerts neuroprotection in a wide range of brain injury models. In the present study, we investigated whether simvastatin could attenuate neurogenetic inhibition and cognitive deficits induced by isoflurane exposure in neonatal rats. Methods: Sprague-Dawley rats at postnatal day (PND) 7 and neural stem cells (NSCs) were treated with either gas mixture, isoflurane, or simvastatin 60 min prior to isoflurane exposure, respectively. The rats were decapitated at PND 8 and PND 10 for detection of neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ) of the hippocampus by immunostaining. NSC proliferation, viability and apoptosis were assessed by immunohistochemistry, CCK-8 and TUNEL, respectively. The protein expressions of caspase-3, p-Akt and p-GSK-3β both in vivo and vitro were assessed by western blotting. Cognitive functions were assessed by Morris Water Maze test and context fear conditioning test at the adult. Results: Isoflurane exposure inhibited neurogenesis in the SVZ and SGZ, decreased NSC proliferation and viability, promoted NSC apoptosis and led to late cognitive deficits. Furthermore, isoflurane increased caspase-3 expression and decreased protein expressions of p-Akt and p-GSK-3β both in vivo and in vitro. Pretreatment with simvastatin attenuated isoflurane-elicited changes in NSCs and cognitive function. Co-treatment with LY294002 reversed the effect of simvastatin on NSCs in vitro. Conclusion: We for the first time showed that simvastatin, by upregulating Akt/GSK-3β signaling pathway, alleviated isoflurane-induced neurogenetic damage and neurocognitive deficits in developing rat brain.
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So, K., T. Moriya, S. Nishitani, H. Takahashi, and K. Shinohara. "The olfactory conditioning in the early postnatal period stimulated neural stem/progenitor cells in the subventricular zone and increased neurogenesis in the olfactory bulb of rats." Neuroscience 151, no. 1 (January 2008): 120–28. http://dx.doi.org/10.1016/j.neuroscience.2007.07.051.
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Chou, Shu-Min, Ke-Xin Li, Ming-Yueh Huang, Chao Chen, Yuan-Hung Lin King, Grant Guangnan Li, Wei Zhou, et al. "Kv1.1 channels regulate early postnatal neurogenesis in mouse hippocampus via the TrkB signaling pathway." eLife 10 (May 21, 2021). http://dx.doi.org/10.7554/elife.58779.
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In the postnatal brain, neurogenesis occurs only within a few regions, such as the hippocampal sub-granular zone (SGZ). Postnatal neurogenesis is tightly regulated by factors that balance stem cell renewal with differentiation, and it gives rise to neurons that participate in learning and memory formation. The Kv1.1 channel, a voltage-gated potassium channel, was previously shown to suppress postnatal neurogenesis in the SGZ in a cell-autonomous manner. In this study, we have clarified the physiological and molecular mechanisms underlying Kv1.1-dependent postnatal neurogenesis. First, we discovered that the membrane potential of neural progenitor cells is highly dynamic during development. We further established a multinomial logistic regression model for cell-type classification based on the biophysical characteristics and corresponding cell markers. We found that the loss of Kv1.1 channel activity causes significant depolarization of type 2b neural progenitor cells. This depolarization is associated with increased tropomyosin receptor kinase B (TrkB) signaling and proliferation of neural progenitor cells; suppressing TrkB signaling reduces the extent of postnatal neurogenesis. Thus, our study defines the role of the Kv1.1 potassium channel in regulating the proliferation of postnatal neural progenitor cells in mouse hippocampus.
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Dou, Zhengchao, Joe Eun Son, and Chi-chung Hui. "Irx3 and Irx5 - Novel Regulatory Factors of Postnatal Hypothalamic Neurogenesis." Frontiers in Neuroscience 15 (November 2, 2021). http://dx.doi.org/10.3389/fnins.2021.763856.
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The hypothalamus is a brain region that exhibits highly conserved anatomy across vertebrate species and functions as a central regulatory hub for many physiological processes such as energy homeostasis and circadian rhythm. Neurons in the arcuate nucleus of the hypothalamus are largely responsible for sensing of peripheral signals such as leptin and insulin, and are critical for the regulation of food intake and energy expenditure. While these neurons are mainly born during embryogenesis, accumulating evidence have demonstrated that neurogenesis also occurs in postnatal-adult mouse hypothalamus, particularly in the first two postnatal weeks. This second wave of active neurogenesis contributes to the remodeling of hypothalamic neuronal populations and regulation of energy homeostasis including hypothalamic leptin sensing. Radial glia cell types, such as tanycytes, are known to act as neuronal progenitors in the postnatal mouse hypothalamus. Our recent study unveiled a previously unreported radial glia-like neural stem cell (RGL-NSC) population that actively contributes to neurogenesis in the postnatal mouse hypothalamus. We also identified Irx3 and Irx5, which encode Iroquois homeodomain-containing transcription factors, as genetic determinants regulating the neurogenic property of these RGL-NSCs. These findings are significant as IRX3 and IRX5 have been implicated in FTO-associated obesity in humans, illustrating the importance of postnatal hypothalamic neurogenesis in energy homeostasis and obesity. In this review, we summarize current knowledge regarding postnatal-adult hypothalamic neurogenesis and highlight recent findings on the radial glia-like cells that contribute to the remodeling of postnatal mouse hypothalamus. We will discuss characteristics of the RGL-NSCs and potential actions of Irx3 and Irx5 in the regulation of neural stem cells in the postnatal-adult mouse brain. Understanding the behavior and regulation of neural stem cells in the postnatal-adult hypothalamus will provide novel mechanistic insights in the control of hypothalamic remodeling and energy homeostasis.
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Ohtsuka, Toshiyuki, and Ryoichiro Kageyama. "Hes1 overexpression leads to expansion of embryonic neural stem cell pool and stem cell reservoir in the postnatal brain." Development 148, no. 4 (February 15, 2021). http://dx.doi.org/10.1242/dev.189191.
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ABSTRACT Neural stem cells (NSCs) gradually alter their characteristics during mammalian neocortical development, resulting in the production of various neurons and glial cells, and remain in the postnatal brain as a source of adult neurogenesis. Notch-Hes signaling is a key regulator of stem cell properties in the developing and postnatal brain, and Hes1 is a major effector that strongly inhibits neuronal differentiation and maintains NSCs. To manipulate Hes1 expression levels in NSCs, we generated transgenic (Tg) mice using the Tet-On system. In Hes1-overexpressing Tg mice, NSCs were maintained in both embryonic and postnatal brains, and generation of later-born neurons was prolonged until later stages in the Tg neocortex. Hes1 overexpression inhibited the production of Tbr2+ intermediate progenitor cells but instead promoted the generation of basal radial glia-like cells in the subventricular zone (SVZ) at late embryonic stages. Furthermore, Hes1-overexpressing Tg mice exhibited the expansion of NSCs and enhanced neurogenesis in the SVZ of adult brain. These results indicate that Hes1 overexpression expanded the embryonic NSC pool and led to the expansion of the NSC reservoir in the postnatal and adult brain.
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Liu, Yubing, Maria Bilen, Marie-Michelle McNicoll, Richard A. Harris, Bensun C. Fong, Mohamed Ariff Iqbal, Smitha Paul, et al. "Early postnatal defects in neurogenesis in the 3xTg mouse model of Alzheimer’s disease." Cell Death & Disease 14, no. 2 (February 18, 2023). http://dx.doi.org/10.1038/s41419-023-05650-1.
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AbstractAlzheimer’s disease (AD) is a progressive neurodegenerative disorder leading to dementia. The hippocampus, which is one of the sites where neural stem cells reside and new neurons are born, exhibits the most significant neuronal loss in AD. A decline in adult neurogenesis has been described in several animal models of AD. However, the age at which this defect first appears remains unknown. To determine at which stage, from birth to adulthood, the neurogenic deficits are found in AD, we used the triple transgenic mouse model of AD (3xTg). We show that defects in neurogenesis are present as early as postnatal stages, well before the onset of any neuropathology or behavioral deficits. We also show that 3xTg mice have significantly fewer neural stem/progenitor cells, with reduced proliferation and decreased numbers of newborn neurons at postnatal stages, consistent with reduced volumes of hippocampal structures. To determine whether there are early changes in the molecular signatures of neural stem/progenitor cells, we perform bulk RNA-seq on cells sorted directly from the hippocampus. We show significant changes in the gene expression profiles at one month of age, including genes of the Notch and Wnt pathways. These findings reveal impairments in neurogenesis very early in the 3xTg AD model, which provides new opportunities for early diagnosis and therapeutic interventions to prevent neurodegeneration in AD.
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Noguchi, Hirofumi, Jesse Garcia Castillo, Kinichi Nakashima, and Samuel J. Pleasure. "Suppressor of fused controls perinatal expansion and quiescence of future dentate adult neural stem cells." eLife 8 (April 11, 2019). http://dx.doi.org/10.7554/elife.42918.
Full textAbstract:
Adult hippocampal neurogenesis requires the quiescent neural stem cell (NSC) pool to persist lifelong. However, establishment and maintenance of quiescent NSC pools during development is not understood. Here, we show that Suppressor of Fused (Sufu) controls establishment of the quiescent NSC pool during mouse dentate gyrus (DG) development by regulating Sonic Hedgehog (Shh) signaling activity. Deletion of Sufu in NSCs early in DG development decreases Shh signaling activity leading to reduced proliferation of NSCs, resulting in a small quiescent NSC pool in adult mice. We found that putative adult NSCs proliferate and increase their numbers in the first postnatal week and subsequently enter a quiescent state towards the end of the first postnatal week. In the absence of Sufu, postnatal expansion of NSCs is compromised, and NSCs prematurely become quiescent. Thus, Sufu is required for Shh signaling activity ensuring expansion and proper transition of NSC pools to quiescent states during DG development.
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Rodríguez-Bodero, Ane, and Juan Manuel Encinas-Pérez. "Does the plasticity of neural stem cells and neurogenesis make them biosensors of disease and damage?" Frontiers in Neuroscience 16 (September 8, 2022). http://dx.doi.org/10.3389/fnins.2022.977209.
Full textAbstract:
Postnatal and adult neurogenesis takes place in the dentate gyrus of the hippocampus in the vast majority of mammals due to the persistence of a population of neural stem cells (NSCs) that also generate astrocytes and more NSCs. These are highly plastic and dynamic phenomena that undergo continuous modifications in response to the changes brain homeostasis. The properties of NSCs as well as the process of neurogenesis and gliogenesis, are reshaped divergently by changes in neuronal activity and by different types of disease and damage. This richness of plastic responses identifies NSCs and newborn neurons as biosensors of the health state of the hippocampus, detecting and providing useful information about processes such as neuronal and network hyperexcitation, excitotoxicity, neurodegeneration, and neuroinflammation. Learning to gather and use this information is a challenge worth of our attention.
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Hwang, William W., Ryan D. Salinas, Jason J. Siu, Kevin W. Kelley, Ryan N. Delgado, Mercedes F. Paredes, Arturo Alvarez-Buylla, Michael C. Oldham, and Daniel A. Lim. "Distinct and separable roles for EZH2 in neurogenic astroglia." eLife 3 (May 27, 2014). http://dx.doi.org/10.7554/elife.02439.
Full textAbstract:
The epigenetic mechanisms that enable specialized astrocytes to retain neurogenic competence throughout adult life are still poorly understood. Here we show that astrocytes that serve as neural stem cells (NSCs) in the adult mouse subventricular zone (SVZ) express the histone methyltransferase EZH2. This Polycomb repressive factor is required for neurogenesis independent of its role in SVZ NSC proliferation, as Ink4a/Arf-deficiency in Ezh2-deleted SVZ NSCs rescues cell proliferation, but neurogenesis remains defective. Olig2 is a direct target of EZH2, and repression of this bHLH transcription factor is critical for neuronal differentiation. Furthermore, Ezh2 prevents the inappropriate activation of genes associated with non-SVZ neuronal subtypes. In the human brain, SVZ cells including local astroglia also express EZH2, correlating with postnatal neurogenesis. Thus, EZH2 is an epigenetic regulator that distinguishes neurogenic SVZ astrocytes, orchestrating distinct and separable aspects of adult stem cell biology, which has important implications for regenerative medicine and oncogenesis.
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Fong, Harmony, and Deborah M. Kurrasch. "Developmental and functional relationships between hypothalamic tanycytes and embryonic radial glia." Frontiers in Neuroscience 16 (January 20, 2023). http://dx.doi.org/10.3389/fnins.2022.1129414.
Full textAbstract:
The hypothalamus is a key regulator of several homeostatic processes, such as circadian rhythms, energy balance, thirst, and thermoregulation. Recently, the hypothalamic third ventricle has emerged as a site of postnatal neurogenesis and gliogenesis. This hypothalamic neural stem potential resides in a heterogeneous population of cells known as tanycytes, which, not unlike radial glia, line the floor and ventrolateral walls of the third ventricle and extend a long process into the hypothalamic parenchyma. Here, we will review historical and recent data regarding tanycyte biology across the lifespan, focusing on the developmental emergence of these diverse cells from embryonic radial glia and their eventual role contributing to a fascinating, but relatively poorly characterized, adult neural stem cell niche.
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Raposo, Ramon da Silva, Daniel Vieira Pinto, Ricardo Moreira, Ronaldo Pereira Dias, Carlos Alberto Fontes Ribeiro, Reinaldo Barreto Oriá, and João Oliveira Malva. "Methylmercury Impact on Adult Neurogenesis: Is the Worst Yet to Come From Recent Brazilian Environmental Disasters?" Frontiers in Aging Neuroscience 12 (November 23, 2020). http://dx.doi.org/10.3389/fnagi.2020.591601.
Full textAbstract:
Worldwide environmental tragedies of anthropogenic origin causing massive release of metals and other pollutants have been increasing considerably. These pollution outbreaks affect the ecosystems and impact human health. Among those tragedies, recent large-scale environmental disasters in Brazil strongly affected riverside populations, leading to high-risk exposure to methylmercury (MeHg). MeHg is highly neurotoxic to the developing brain. This toxicant causes neural stem cell dysfunction and neurodevelopmental abnormalities. However, less is known about the effects of MeHg in the postnatal neurogenic niche, which harbors neural stem cells and their progeny, in the adult brain. Therefore, taking in consideration the impact of MeHg in human health it is urgent to clarify possible associations between exposure to mercury, accelerated cognitive decline, and neurodegenerative diseases. In this perspectives paper, we discuss the neurotoxic mechanisms of MeHg on postnatal neurogenesis and the putative implications associated with accelerated brain aging and early-onset cognitive decline in populations highly exposed to this environmental neurotoxicant.
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Serra-Almeida, Catarina, Cláudia Saraiva, Marta Esteves, Raquel Ferreira, Tiago Santos, Ana Clara Cristóvão, and Liliana Bernardino. "C-Terminal Binding Proteins Promote Neurogenesis and Oligodendrogenesis in the Subventricular Zone." Frontiers in Cell and Developmental Biology 8 (January 6, 2021). http://dx.doi.org/10.3389/fcell.2020.584220.
Full textAbstract:
C-terminal binding proteins (CtBPs) are transcriptional modulators that can regulate gene expression through the recruitment of a corepressor complex composed of chromatin-modifying enzymes and transcriptional factors. In the brain, CtBPs have been described as regulators of cell proliferation, differentiation, and survival. Nevertheless, the role of CtBPs on postnatal neural stem cells (NSCs) fate is not known yet. Herein, we evaluate the expression and functions of CtBPs in postnatal NSCs from the subventricular zone (SVZ). We found that CtBPs were expressed in immature/progenitor cells, neurons and glial cells in the SVZ niche. Using the CtBPs modulator 4-methylthio 2-oxobutyric acid (MTOB), our results showed that 1 mM of MTOB induced cell death, while 5, 25, and 50 μM increased the number of proliferating neuroblasts, mature neurons, and oligodendrocytes. Interestingly, it also increased the dendritic complexity of immature neurons. Altogether, our results highlight CtBPs putative application for brain regenerative applications.