Neurogenesis after Primary Intracerebral Hemorrhage in Adult Human Brain

Shen, Jianfeng; Xie, Lin; Mao, Xiao‐Ming; Zhou, Yong‐Qing; Zhan, Renya; Greenberg, David A.; Jin, Kunlin

doi:10.1038/jcbfm.2008.37

Cited by 65 publications

(54 citation statements)

References 39 publications

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“…Indeed, the hippocampal formation has many monosynaptic connections with several amygdala nuclei, including those that have shown changes in neuron number (18)(19)(20)(21). Although lesion-induced migration of neurons was previously suggested in primates (7,9,37), the integration of these neurons was never quantified and appeared to be limited to the immediate area surrounding the lesion site. Because of the existence of a local population of immature neurons and the evidence that many of them mature in the course of postnatal development (10), the amygdala may be a particularly favorable environment for the integration of immature neurons into functional circuits.…”

Section: Differentiation Of Immature Neuronsmentioning

confidence: 96%

Selective lesion of the hippocampus increases the differentiation of immature neurons in the monkey amygdala

Chareyron

Amaral

Lavenex

2016

Proc. Natl. Acad. Sci. U.S.A.

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A large population of immature neurons is present in the ventromedial portion of the adult primate amygdala, a region that receives substantial direct projections from the hippocampal formation. Here, we show the effects of neonatal (n = 8) and adult (n = 6) hippocampal lesions on the populations of mature and immature neurons in the paralaminar, lateral, and basal nuclei of the adult monkey amygdala. Compared with unoperated controls (n = 7), the number of mature neurons was about 70% higher in the paralaminar nucleus of neonate-and adult-lesioned monkeys, and 40% higher in the lateral and basal nuclei of neonate-lesioned monkeys. The number of immature neurons in the paralaminar nucleus was 40% higher in neonate-lesioned monkeys and 30% lower in adult-lesioned monkeys. Similar changes in neuron numbers were also found in two monkeys with nonexperimental, selective, bilateral hippocampal damage. These changes in neuron numbers following hippocampal lesions appear to reflect the differentiation of immature neurons present in the paralaminar nucleus. After adult lesions, the differentiation of immature neurons was essentially restricted to the paralaminar nucleus and was associated with a decrease in the population of immature neurons. In contrast, after neonatal lesions, the differentiation of immature neurons involved the paralaminar, lateral, and basal nuclei. It was associated with an increase in the population of immature neurons in the paralaminar nucleus. Such lesion-induced neuronal plasticity sheds new light on potential mechanisms that may facilitate functional recovery following focal brain injury.immature neuron | migration | subventricular zone | plasticity | neurodevelopmental disorders P revious studies have shown the existence of cells expressing markers typically associated with immature neurons in various regions of the adult mammalian brain (1-5), which suggested a strong potential for neuronal plasticity following focal brain injury in adult individuals (6-9). One such brain region that contains a large population of immature neurons at birth is situated along the temporal horn of the lateral ventricle and includes the paralaminar nucleus of the amygdala in monkeys (3, 10, 11) and humans (5). These immature neurons are positive for Bcl2, class III β-tubulin, doublecortin (DCX), and polysialylated neural cell adhesion molecule (PSA-NCAM) (3,(12)(13)(14)(15). In monkeys, the population of immature neurons present in the paralaminar nucleus at birth decreases after 1 y of age (10). At the same time, the number of mature neurons increases, thus suggesting that neuronal differentiation occurs in the amygdala over a prolonged course of postnatal development. However, a large population of immature-looking neurons remains into adulthood (10). Additionally, although a number of cellular mechanisms involved in the regulation of postnatal neurogenesis in neurogenic brain regions have been identified (16), the specific factors that may induce the differentiation of immature neurons in nonneurogenic regio...

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Section: Differentiation Of Immature Neuronsmentioning

confidence: 96%

Selective lesion of the hippocampus increases the differentiation of immature neurons in the monkey amygdala

Chareyron

Amaral

Lavenex

2016

Proc. Natl. Acad. Sci. U.S.A.

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“…MNCs, in particular, not only modulate inflammatory and immunemediated responses but also upregulate various aspects of repair in rodents with ischemic stroke. One aspect of brain repair may be the migration of neuroblasts toward the damaged area, which has been shown to occur in the blood injection rat ICH model and possibly in the brains of patients after ICH [47]. There may be some concordance between neurogenesis and functional improvement after brain injury [48].…”

Section: Discussionmentioning

confidence: 99%

Autologous Bone Marrow Mononuclear Cells Exert Broad Effects on Short- and Long-Term Biological and Functional Outcomes in Rodents with Intracerebral Hemorrhage

Suda

Yang²,

Schaar³

et al. 2015

Stem Cells and Development

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Autologous bone marrow-derived mononuclear cells (MNCs) are a potential therapy for ischemic stroke. However, the effect of MNCs in intracerebral hemorrhage (ICH) has not been fully studied. In this study, we investigated the effects of autologous MNCs in experimental ICH. ICH was induced by infusion of autologous blood into the left striatum in young and aged male Long Evans rats. Twenty-four hours after ICH, rats were randomized to receive an intravenous administration of autologous MNCs (1 · 10 7 cells/kg) or saline. We examined brain water content, various markers related to the integrity of the neurovascular unit and inflammation, neurological deficit, neuroregeneration, and brain atrophy. We found that MNC-treated young rats showed a reduction in the neurotrophil infiltration, the number of inducible nitric oxide synthase-positive cells, and the expression of inflammatory-related signalings such as the high-mobility group protein box-1, S100 calcium binding protein B, matrix metalloproteinase-9, and aquaporin 4. Ultimately, MNCs reduced brain edema in the perihematomal area compared with saline-treated animals at 3 days after ICH. Moreover, MNCs increased vessel density and migration of doublecortin-positive cells, improved motor functional recovery, spatial learning, and memory impairment, and reduced brain atrophy compared with saline-treated animals at 28 days after ICH. We also found that MNCs reduced brain edema and brain atrophy and improved spatial learning and memory in aged rats after ICH. We conclude that autologous MNCs can be safely harvested and intravenously reinfused in rodent ICH and may improve long-term structural and functional recovery after ICH. The results of this study may be applicable when considering future clinical trials testing MNCs for ICH.

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“…This finding, however, may depend upon initial insult severity, which appears in those studies to be less than that presently used. One must also consider the possiblity that ICH-induced neurogenesis (Masuda et al, 2007;Shen et al, 2008) confound these results at the 60-day survival time if some new neurons were stained with Golgi-Cox and assessed in this study.…”

Section: Discussionmentioning

confidence: 99%

Progressive Brain Damage and Alterations in Dendritic Arborization after Collagenase-Induced Intracerebral Hemorrhage in Rats

Nguyen¹,

Huynh²,

Sjovold³

et al. 2008

CNR

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Intracerebral hemorrhage (ICH) was widely believed to be a monophasic event whereby cell death occurs from the initial space-occupying effects of the hematoma. However, we now know that secondary degenerative events contribute to delayed cell death, functional impairment and clinical deterioration. In three experiments, we further characterized the long-term maturation of injury in the collagenase model of striatal ICH in rat. First, we quantified the volume of tissue lost from 7 to 60 days showing that tissue loss more than doubled over this time. As the volume of tissue lost does not distinguish gray from white matter damage, gold chloride staining was used in a second experiment in ICH rats that survived 7 or 60 days. The mid-sagittal area of the corpus callosum significantly declined (22%) over this period, whereas the hippocampal and anterior commissures were not affected. A third experiment used the Golgi-Cox stain to examine dendritic arborization of peri-hematoma and contralateral medium spiny neurons of the striatum. We found an early and sustained increase in dendritic arborization in the non-lesioned hemisphere, whereas there was initial atrophy of peri-hematoma striatal neurons that eventually recovered to normal. These findings show that tissue loss, including white matter atrophy, continues over extended periods after ICH making it a potential target for cytoprotective agents. Finally, the dendritic alterations in both ipsi-and contralateral striatal neurons likely influence spontaneous recovery and are potential targets to further improve it.

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Neurogenesis after Primary Intracerebral Hemorrhage in Adult Human Brain

Cited by 65 publications

References 39 publications

Selective lesion of the hippocampus increases the differentiation of immature neurons in the monkey amygdala

Selective lesion of the hippocampus increases the differentiation of immature neurons in the monkey amygdala

Autologous Bone Marrow Mononuclear Cells Exert Broad Effects on Short- and Long-Term Biological and Functional Outcomes in Rodents with Intracerebral Hemorrhage

Progressive Brain Damage and Alterations in Dendritic Arborization after Collagenase-Induced Intracerebral Hemorrhage in Rats

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