Differential neurogenesis and gliogenesis by local and migrating neural stem cells in the olfactory bulb

Fukushima, Nanae; Yokouchi, Kumiko; Kawagishi, Kyutaro; Moriizumi, Tetsuji

doi:10.1016/s0168-0102(02)00173-6

Cited by 34 publications

(30 citation statements)

References 28 publications

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“…This population may correspond to the NeuN ϩ cells that we see in gr s , and one would predict that resulting periglomerular neurons might also be NeuN ϩ . However, in our study, we failed to identify NeuN ϩ neurons within the glomerular layer, as has been reported previously in rats carrying lesions in the RMS (Fukushima et al, 2002). Several possible scenarios may explain the absence of NeuN ϩ cells in the periglomerular layer: (1) periglomerular progenitor neurons may be more sensitive to the apoptotic effects of infection compared with granule cells, and these cells may die before reaching the periglomerular cell layer; or (2) infection of neuronal progenitor cells may influence the differentiation of these cells, thereby causing all migratory neuroblasts to differentiate preferentially into granule cells, which reside in gr d .…”

Section: Discussionsupporting

confidence: 68%

Coxsackievirus Targets Proliferating Neuronal Progenitor Cells in the Neonatal CNS

Feuer¹,

Pagarigan²,

Harkins³

et al. 2005

J. Neurosci.

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Type B coxsackieviruses (CVB) frequently infect the CNS and, together with other enteroviruses, are the most common cause of viral meningitis in humans. Newborn infants are particularly vulnerable, and CVB also can infect the fetus, leading to mortality, or to neurodevelopmental defects in surviving infants. Using a mouse model of neonatal CVB infection, we previously demonstrated that coxsackievirus B3 (CVB3) could infect neuronal progenitor cells in the subventricular zone (SVZ). Here we extend these findings, and we show that CVB3 targets actively proliferating (bromodeoxyuridine ϩ , Ki67 ϩ ) cells in the SVZ, including type B and type A stem cells. However, infected cells exiting the SVZ have lost their proliferative capacity, in contrast to their uninfected companions. Despite being proliferation deficient, the infected neuronal precursors could migrate along the rostral migratory stream and radial glia, to reach their final destinations in the olfactory bulb or cerebral cortex. Furthermore, infection did not prevent cell differentiation, as determined by cellular morphology and the expression of maturation markers. These data lead us to propose a model of CVB infection of the developing CNS, which may explain the neurodevelopmental defects that result from fetal infection.

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Section: Discussionsupporting

confidence: 68%

Coxsackievirus Targets Proliferating Neuronal Progenitor Cells in the Neonatal CNS

Feuer¹,

Pagarigan²,

Harkins³

et al. 2005

J. Neurosci.

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“…These numbers probably underestimate the number of JG cells and overestimate the number of tufted cells. First, about half of the neurons in the GL were not counted due to poor staining with NeuN probably because of either degradation in the course of experiment or the immature state of newly developing neurons (Coskun and Luskin, 2002;Fukushima et al, 2002;Winner et al, 2002). Second, some EPL cells are local interneurons with short dendrites (Hamilton et al, 2005), therefore the actual number of tufted cells per glomerulus is likely to be lower than in our count.…”

Section: Morphological Substrate Of Sglfpsmentioning

confidence: 85%

Spontaneous field potentials in the glomeruli of the olfactory bulb: The leading role of juxtaglomerular cells

et al. 2006

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Field potentials recorded in the olfactory bulb glomerular layer (GL) are thought to result mainly from activation of mitral and tufted cells. The contribution of juxtaglomerular cells (JG) is unknown. We tested the hypothesis that JG are the main driving force to novel spontaneous glomerular layer field potentials (sGLFPs), which were recorded in rat olfactory bulb slices maintained in an interface chamber. We found that sGLFPs have comparable magnitudes, durations and frequencies both in standard horizontal slices, where all layers with all cell types were present, and in isolated GL slices, where only JG cells were preserved. Hence, the impact of mitral and deep/medium tufted cells to sGLFPs turned out to be minor. Therefore, we propose that the main generators of sGLFPs are JG neurons. We further explored the mechanism of generation of sGLFPs using a neuronal ensemble model comprising all types of cells associated with a single glomerulus. Random orientation and homogenous distribution of dendrites in the glomerular neuropil along with surrounding shell of cell bodies of JG neurons resulted in substantial spatial restriction of the generated field potential. The model predicts that less than 20% of sGLFP can spread from one glomerulus to an adjacent one. The contribution of JG cells to the total field in the center of the glomerulus is estimated as ~50% (~34% periglomerular and ~16% external tufted cells), whereas deep/medium tufted cells provide ~39% and mitral cells only ~10%. Occasionally, some sGLFPs recorded in adjacent or remote glomeruli were cross-correlated, suggesting involvement of interglomerular communication in information coding. These results demonstrate a leading role of JG cells in activation of the main olfactory bulb (MOB) functional modules. Finally, we hypothesize that the GL is not a set of independent modules, but it represents a subsystem in the MOB network, which can perform initial processing of odors. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2008 May 13. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptField potentials recorded in brain tissue are generated by summation of electrical fields' f neuronal dipoles (Lorente de Nó, 1947;Buresh et al., 1962;Hubbard et al., 1969;Guselnikov, 1976; Karnup, 1980 Karnup, , 1982. Synchronous fluctuations of electrical charges on similarly oriented ends of dipoles, for instance in apical dendrites of pyramidal cells in the hippocampus or neocortex, result in electroencephalographic (EEG) waves. In brain structures, lacking comparable orientation of neuronal dipoles or constructed of quadrupole-like multipolar neurons, a distinctive EEG cannot be recorded (Buresh et al., 1962;Guselnikov, 1976). In layered structures, such as the hippocampus and neocortex, current source density analysis can determine where the majority of synchronously depolarized neuronal compartments are located (for a review, see Mitzdorf, 1985). An active zone (in which neurons are depolarized by ...

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“…It has been demonstrated that NSPCs proliferate in the subventricular zone (SVZ) and migrate tangentially through the SVZ, in a pattern reminiscent of the rostral migratory stream (RMS), toward the olfactory bulb where they differentiate into mature neurons (4)(5)(6). It has also been recently demonstrated that NSPCs migrate to sites of pathological insult such as various types of brain injury (i.e., ischemia and blunt trauma) and tumors (7)(8)(9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Neuronally expressed stem cell factor induces neural stem cell migration to areas of brain injury

2004

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Neural stem/progenitor cell (NSPC) migration toward sites of damaged central nervous system (CNS) tissue may represent an adaptive response for the purpose of limiting and/or repairing damage. Little is known of the mechanisms responsible for this migratory response. We constructed a cDNA library of injured mouse forebrain using subtractive suppression hybridization (SSH) to identify genes that were selectively upregulated in the injured hemisphere. We demonstrate that stem cell factor (SCF) mRNA and protein are highly induced in neurons within the zone of injured brain. Additionally, the SCF receptor c-kit is expressed on NSPCs in vitro and in vivo. Finally, we demonstrate that recombinant SCF induces potent NSPC migration in vitro and in vivo through the activation of c-kit on NSPCs. These data suggest that the SCF/c-kit pathway is involved in the migration of NSPCs to sites of brain injury and that SCF may prove useful for inducing progenitor cell recruitment to specific areas of the CNS for cell-based therapeutic strategies.

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Differential neurogenesis and gliogenesis by local and migrating neural stem cells in the olfactory bulb

Cited by 34 publications

References 28 publications

Coxsackievirus Targets Proliferating Neuronal Progenitor Cells in the Neonatal CNS

Coxsackievirus Targets Proliferating Neuronal Progenitor Cells in the Neonatal CNS

Spontaneous field potentials in the glomeruli of the olfactory bulb: The leading role of juxtaglomerular cells

Neuronally expressed stem cell factor induces neural stem cell migration to areas of brain injury

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