Stem Cells in Neurodevelopment and Plasticity

Vaccarino, Flora M.; Ganat, Yosif; Zhang, Yuchun; Zheng, Wei

doi:10.1016/s0893-133x(01)00349-9

Cited by 51 publications

(42 citation statements)

References 99 publications

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“…The dorsal PVE is composed of radially oriented progenitors that guide their neuronal progeny to topographically corresponding regions of the developing neocortex (Rakic, 1988;Noctor et al, 2001). Fgf2 and Fgf receptor 1 are both expressed by these radially oriented progenitor cells in an anteroposterior decreasing gradient (Wilke et al, 1997;Vaccarino et al, 1999;Raballo et al, 2000;Ragsdale et al, 2000;Vaccarino et al, 2001), suggesting that Fgf2 is a paracrine signal for these cells. To find out whether Fgf2 regulates progenitor cell division preferentially in anterior regions of the PVE, we examined sections from wild-type and Fgf2 knockout animals in which the whole population of constitutively proliferating cells was labeled by cumulative bromodeoxyuridine (BrdU) injections for 8 hr (Raballo et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Fibroblast Growth Factor 2 Is Necessary for the Growth of Glutamate Projection Neurons in the Anterior Neocortex

et al. 2002

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Basic fibroblast growth factor (Fgf2) is required for the generation of founder cells within the dorsal pseudostratified ventricular epithelium, which will generate the cerebral cortex, but the ganglionic eminences are not affected. We report here that the Fgf2 null mutant mice show an ϳ40% decrease in cortical glutamatergic pyramidal neurons. In contrast, no change in pyramidal or granule cell number is detected in the hippocampus of Fgf2 Ϫ/Ϫ mice. In addition, the soma of the pyramidal cells in the frontal and parietal cortices are smaller in Fgf2 knock-out mice. The decrease in the number and size of glutamatergic neuronal population affects all cortical layers but is restricted to the frontal and parietal cortices without any change in the occipital cortex, indicating that Fgf2 is necessary to regulate cell number and size in the anterior cerebral cortex. In contrast to pyramidal neurons, cortical GABA interneurons are unaffected by the lack of Fgf2. The resulting imbalance between the excitatory and inhibitory neurotransmission in the cerebral cortex is reflected by an increased duration of sleep when the animals receive a GABA receptor agonist. Thus, Fgf2 signaling may contribute to the regional specification of the cerebral cortex and may play a role in increasing the size of anterior cortical regions during vertebrate evolution.

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Section: Discussionmentioning

confidence: 99%

Fibroblast Growth Factor 2 Is Necessary for the Growth of Glutamate Projection Neurons in the Anterior Neocortex

et al. 2002

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“…Adult neuronal cultures, compared to those taken from developing brain tissue, are phenotypically distinct. Developing neurons display different patterns of neuroplasticityrelated gene expression, molecular changes and morphological responses to neurotrophic proteins and neurotransmitters, and increased survivability in nonphysiologic environments (Schwartz, 1992;Penn, 2001;Vaccarino et al, 2001;Nottebohm, 2002). In hippocampal preparations, newly generated DG neurons undergo LTP more readily, and are insensitive to GABAergic inhibition of LTP compared to putative mature DG neurons (Snyder et al, 2001).…”

Section: General Informatic Effects Of Simulated Turnovermentioning

confidence: 99%

Simulated Apoptosis/Neurogenesis Regulates Learning and Memory Capabilities of Adaptive Neural Networks

Chambers

Potenza

Hoffman

et al. 2003

Neuropsychopharmacol

140

107

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Characterization of neuronal death and neurogenesis in the adult brain of birds, humans, and other mammals raises the possibility that neuronal turnover represents a special form of neuroplasticity associated with stress responses, cognition, and the pathophysiology and treatment of psychiatric disorders. Multilayer neural network models capable of learning alphabetic character representations via incremental synaptic connection strength changes were used to assess additional learning and memory effects incurred by simulation of coordinated apoptotic and neurogenic events in the middle layer. Using a consistent incremental learning capability across all neurons and experimental conditions, increasing the number of middle layer neurons undergoing turnover increased network learning capacity for new information, and increased forgetting of old information. Simulations also showed that specific patterns of neural turnover based on individual neuronal connection characteristics, or the temporal-spatial pattern of neurons chosen for turnover during new learning impacts new learning performance. These simulations predict that apoptotic and neurogenic events could act together to produce specific learning and memory effects beyond those provided by ongoing mechanisms of connection plasticity in neuronal populations. Regulation of rates as well as patterns of neuronal turnover may serve an important function in tuning the informatic properties of plastic networks according to novel informational demands. Analogous regulation in the hippocampus may provide for adaptive cognitive and emotional responses to novel and stressful contexts, or operate suboptimally as a basis for psychiatric disorders. The implications of these elementary simulations for future biological and neural modeling research on apoptosis and neurogenesis are discussed.

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“…[3][4][5][6][7][8] In the adult brain, there are three major phases of expansion and differentiation during neurogenesis: the asymmetric division of stem cells to generate a small number of transit amplifying cells, the rapid proliferation of transit amplifying cells to produce a larger population of neuronal precursors, and the commitment of these precursors to a neuronal fate. 2,9,10 Major unresolved questions entail how extrinsic factors work together to produce specific precursor populations, and how these precursors attain different maturational fates upon cell cycle exit.…”

Section: Introductionmentioning

confidence: 99%

“…In the brain, stem cells display slower cell cycle kinetics than their progeny. 2 Following proliferation, and in the absence of the addition of other factors, NGF treated cells undergo increased apoptosis while those treated with BDNF become quiescent.…”

Section: Introductionmentioning

confidence: 99%

Progressive and Inhibitory Cell Cycle Proteins Act Simultaneously to Regulate Neurotrophin-mediated Proliferation and Maturation of Neuronal Precursors

Simpson

Moon²,

Kleman

et al. 2007

Cell Cycle

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ACKnowlEdGEMEntSWe thank Amy Palmer for helpful discussions and reading of the manuscript, and Susan McTeer for manuscript preparation. This work was supported by grants NIDCD RO3 DC005704 to P.J.S., NIDCD RO1 DC02979 and NINDS RO1 NS39657 to G.V.R. AbStRACtNeuronal stem cell expansion and differentiation is a process involving stages of proliferation and maturation governed by the sequential and combinatorial exposure of cells to extrinsic factors. The olfactory epithelium is an excellent model to investigate regulation of this process, as it undergoes neuronal replacement post-natally. We have shown that the neurotrophins NGF and BDNF sequentially promote proliferation of developing olfactory sensory neuronal precursors, although their kinetics of proliferation and cell fate outcomes differ. Interestingly, CNP inhibits this neurotrophin-induced proliferation and promotes the maturation of these precursors to their next developmental stage. Here, we investigate the mechanisms behind these actions. Both NGF and BDNF increase the expression of cyclin D1 and cyclin-dependent kinase 4 (cdk4), with temporal expression patterns that parallel the proliferation kinetics of their cellular targets. The timing of cyclin D1 expression reflects differences in the need for transcription and translation in early and late stage precursors. CNP inhibits neurotrophin-induced cyclin D1 expression, and induces the expression of different profiles of inhibitory cell cycle proteins, which are neurotrophin-specific and correlate with the attainment of different maturational cell fates. Inhibition of protein degradation reverses the effects of neurotrophins and CNP on cyclin D1 and inhibitor expression levels, respectively. These results suggest a model for cell cycle regulation that involves the simultaneous expression of progressive and inhibitory cell cycle regulatory proteins in response to both proliferation and differentiation agents, followed by selective degradation of these proteins, providing a mechanism for rapid and exquisite control of the cell cycle.

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Stem Cells in Neurodevelopment and Plasticity

Cited by 51 publications

References 99 publications

Fibroblast Growth Factor 2 Is Necessary for the Growth of Glutamate Projection Neurons in the Anterior Neocortex

Fibroblast Growth Factor 2 Is Necessary for the Growth of Glutamate Projection Neurons in the Anterior Neocortex

Simulated Apoptosis/Neurogenesis Regulates Learning and Memory Capabilities of Adaptive Neural Networks

Progressive and Inhibitory Cell Cycle Proteins Act Simultaneously to Regulate Neurotrophin-mediated Proliferation and Maturation of Neuronal Precursors

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