Sustained neocortical neurogenesis after neonatal hypoxic/ischemic injury

Yang, Zhengang; Covey, Matthew; Bitel, Claudine L.; Ni, Li; Jonakait, G. Miller; Levison, Steven W.

doi:10.1002/ana.21068

Cited by 147 publications

(143 citation statements)

References 37 publications

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“…Recent evidence indicates that neurogenesis persists beyond the fetal period and into adulthood in certain areas of the brain including the subventricular zone of the lateral ventricles and the subgranular zone of the dentate gyrus of the hippocampus [Toni et al, 2008]. In neonatal rats with experimental hypoxic-ischemic injury, sustained neurogenesis persists in the subventricular zone for months after injury and continues to populate the cerebral cortex with new neurons [Yang et al, 2007]. A similar phenomenon has been shown to occur in adult rodents after stroke [Lichtenwalner and Parent, 2006].…”

Section: Mechanisms For Plasticity In the Central Nervous Systemmentioning

confidence: 84%

Plasticity in the developing brain: Implications for rehabilitation

Johnston

2009

Dev Disabil Res Revs

442

273

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Neuronal plasticity allows the central nervous system to learn skills and remember information, to reorganize neuronal networks in response to environmental stimulation, and to recover from brain and spinal cord injuries. Neuronal plasticity is enhanced in the developing brain and it is usually adaptive and beneficial but can also be maladaptive and responsible for neurological disorders in some situations. Basic mechanisms that are involved in plasticity include neurogenesis, programmed cell death, and activity-dependent synaptic plasticity. Repetitive stimulation of synapses can cause long-term potentiation or long-term depression of neurotransmission. These changes are associated with physical changes in dendritic spines and neuronal circuits. Overproduction of synapses during postnatal development in children contributes to enhanced plasticity by providing an excess of synapses that are pruned during early adolescence. Clinical examples of adaptive neuronal plasticity include reorganization of cortical maps of the fingers in response to practice playing a stringed instrument and constraint-induced movement therapy to improve hemiparesis caused by stroke or cerebral palsy. These forms of plasticity are associated with structural and functional changes in the brain that can be detected with magnetic resonance imaging, positron emission tomography, or transcranial magnetic stimulation (TMS). TMS and other forms of brain stimulation are also being used experimentally to enhance brain plasticity and recovery of function. Plasticity is also influenced by genetic factors such as mutations in brain-derived neuronal growth factor. Understanding brain plasticity provides a basis for developing better therapies to improve outcome from acquired brain injuries. ' 2009 Wiley-Liss, Inc. Dev Disabil Res Rev 200915:94-101.

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Section: Mechanisms For Plasticity In the Central Nervous Systemmentioning

confidence: 84%

Plasticity in the developing brain: Implications for rehabilitation

Johnston

2009

Dev Disabil Res Revs

442

273

View full text Add to dashboard Cite

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“…Accumulating evidence suggests that HI injury promotes extensive cell proliferation in the SVZ of the rodent brain. 14,[77][78][79][80][81][82][83] Several studies in which P6 and P7 rats and P10 mice were subjected to moderate HI showed that the SVZ expands in size, illustrated by increased cresyl-violet staining and nestin-positive cells in the ipsilateral SVZ. 78,79,83 Furthermore, an increase in BrdU þ cells was observed in the affected SVZ from 1 week to 3 weeks after HI, implying that cell proliferation is stimulated in this region.…”

Section: Neurogenesis After a Hypoxic-ischemic Insultmentioning

confidence: 99%

“…Several studies observed a significant increase in Dcx/BrdU double-positive cells in the SVZ, striatum, and cortex from 1 to 4 weeks after injury. 77,79,[81][82][83] These double-positive cells were clustered in chains in the striatum and cortex and displayed the morphology of migrating neuroblasts. [82][83][84] Studies investigating the differentiation rate of proliferating cells into neurons and their survival show contradicting results.…”

Section: Cell-fate Commitment Of Proliferating Cells In the Subgranulmentioning

confidence: 99%

“…77,79,[81][82][83] These double-positive cells were clustered in chains in the striatum and cortex and displayed the morphology of migrating neuroblasts. [82][83][84] Studies investigating the differentiation rate of proliferating cells into neurons and their survival show contradicting results. Current data show a decrease, 14,78 increase, 83,84 or no change (cortical area) 14 in NeuN/BrdU double-labeled cells compared with healthy brains.…”

Section: Cell-fate Commitment Of Proliferating Cells In the Subgranulmentioning

confidence: 99%

“…79 Furthermore, only 15% of newly generated neurons in the cortex survived 5 weeks after HI. 82 The authors proposed that newborn neurons mature slowly, 83 raising the possibility that the failure to detect NeuN/BrdU-positive cells in previous studies 78,79 may be because of the relatively short period of time elapsed (2 to 3 weeks) after BrdU injection. Yet, prolonging the interval after BrdU administration may also lead to negative results, as the low number of newborn neurons could be the consequence of both slow maturation and impaired survival of neuroblasts.…”

Section: Cell-fate Commitment Of Proliferating Cells In the Subgranulmentioning

confidence: 99%

See 2 more Smart Citations

The Endogenous Regenerative Capacity of the Damaged Newborn Brain: Boosting Neurogenesis with Mesenchymal Stem Cell Treatment

Donega

Velthoven

Nijboer

et al. 2013

J Cereb Blood Flow Metab

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Neurogenesis continues throughout adulthood. The neurogenic capacity of the brain increases after injury by, e.g., hypoxiaischemia. However, it is well known that in many cases brain damage does not resolve spontaneously, indicating that the endogenous regenerative capacity of the brain is insufficient. Neonatal encephalopathy leads to high mortality rates and long-term neurologic deficits in babies worldwide. Therefore, there is an urgent need to develop more efficient therapeutic strategies. The latest findings indicate that stem cells represent a novel therapeutic possibility to improve outcome in models of neonatal encephalopathy. Transplanted stem cells secrete factors that stimulate and maintain neurogenesis, thereby increasing cell proliferation, neuronal differentiation, and functional integration. Understanding the molecular and cellular mechanisms underlying neurogenesis after an insult is crucial for developing tools to enhance the neurogenic capacity of the brain. The aim of this review is to discuss the endogenous capacity of the neonatal brain to regenerate after a cerebral ischemic insult. We present an overview of the molecular and cellular mechanisms underlying endogenous regenerative processes during development as well as after a cerebral ischemic insult. Furthermore, we will consider the potential to use stem cell transplantation as a means to boost endogenous neurogenesis and restore brain function.

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Replacing neocortical neurons after stroke

Parent

Silverstein

2007

Annals of Neurology

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Sustained neocortical neurogenesis after neonatal hypoxic/ischemic injury

Cited by 147 publications

References 37 publications

Plasticity in the developing brain: Implications for rehabilitation

Plasticity in the developing brain: Implications for rehabilitation

The Endogenous Regenerative Capacity of the Damaged Newborn Brain: Boosting Neurogenesis with Mesenchymal Stem Cell Treatment

Replacing neocortical neurons after stroke

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