scholarly journals Neural precursor cells are decreased in the hippocampus of the delayed carbon monoxide encephalopathy rat model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shinichiro Ochi ◽  
Keisuke Sekiya ◽  
Naoki Abe ◽  
Yu Funahashi ◽  
Hiroshi Kumon ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Cognitive Impairment ◽  
Rat Model ◽  
Cell Number ◽  
Lipid Binding ◽  
Precursor Cells ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Neural Precursor Cells ◽  
Neural Precursor

AbstractThe pathophysiology of delayed carbon monoxide (CO) encephalopathy remains unclear. In this study, the effects of CO exposure on the dentate gyrus (DG) were investigated in a Wistar rat model by histochemical and molecular methods. Model rats showed significant cognitive impairment in the passive-avoidance test beginning 7 days after CO exposure. Immunohistochemistry showed that compared to the control, the cell number of SRY (sex-determining region Y)-box 2 (SOX2)+/brain lipid binding protein (BLBP)+/glial fibrillary acidic protein (GFAP)+ cells in the DG was significantly less, but the number of SOX2+/GFAP− cells was not, reflecting a decreased number of type 1 and type 2a neural precursor cells. Compared to the control, the numbers of CD11b+ cells and neuron glial antigen 2+ cells were significantly less, but the number of SOX2−/GFAP+ cells was not. Flow cytometry showed that the percent of live microglial cells isolated from the hippocampus in this CO rat model was significantly lower than in controls. Furthermore, mRNA expression of fibroblast growth factor 2 and glial cell-derived neurotrophic factor, which are neurogenic factors, was significantly decreased in that area. We conclude that, in this rat model, there is an association between delayed cognitive impairment with dysregulated adult hippocampal neurogenesis and glial changes in delayed CO encephalopathy.

scholarly journals Sustained IL-1β expression impairs adult hippocampal neurogenesis independent of IL-1 signaling in nestin+ neural precursor cells

2013 ◽  
Vol 32 ◽  
pp. 9-18 ◽  
Author(s):  
Michael D. Wu ◽  
Sara L. Montgomery ◽  
Fatima Rivera-Escalera ◽  
John A. Olschowka ◽  
M. Kerry O’Banion
Keyword(s):  
Precursor Cells ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Neural Precursor Cells ◽  
Neural Precursor

Comparison of the therapeutic potential of adult and embryonic neural precursor cells in a rat model of Parkinson disease

2008 ◽  
Vol 108 (1) ◽  
pp. 149-159 ◽  
Author(s):  
Kenichiro Muraoka ◽  
Tetsuro Shingo ◽  
Takao Yasuhara ◽  
Masahiro Kameda ◽  
Wen Ji Yuen ◽  
...  
Keyword(s):  
Parkinson Disease ◽  
Rat Model ◽  
Fluorescent Protein ◽  
Therapeutic Potential ◽  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Therapeutic Effects ◽  
Adenoviral Infection

Object The therapeutic effects of adult and embryonic neural precursor cells (NPCs) were evaluated and their therapeutic potential compared in a rat model of Parkinson disease. Methods Adult NPCs were obtained from the subventricular zone and embryonic NPCs were taken from the ganglionic eminence of 14-day-old embryos. Each NPC type was cultured with epidermal growth factor. The in vitro neuronal differentiation rate of adult NPCs was approximately equivalent to that of embryonic NPCs after two passages. Next, the NPCs were transfected with either green fluorescent protein or glial cell line–derived neurotrophic factor (GDNF) by adenoviral infection and transplanted into the striata in a rat model of Parkinson disease (PD) induced by unilateral intrastriatal injection of 6-hydroxydopamine. An amphetamine-induced rotation test was used to evaluate rat behavioral improvement, and immunohistochemical analysis was performed to compare grafted cell survival, differentiation, and host tissue changes. Results The rats with GDNF-transfected NPCs had significantly fewer amphetamine-induced rotations and less histological damage. Except for the proportion of surviving grafted cells, there were no significant differences between adult and embryonic NPCs. Conclusions Adult and embryonic NPCs have a comparable therapeutic potential in a rat model of PD.

scholarly journals Transplantation of Human Neural Precursor Cells Reverses Syrinx Growth in a Rat Model of Post-Traumatic Syringomyelia

2021 ◽  
Author(s):  
Ning Xu ◽  
Tingting Xu ◽  
Raymond Mirasol ◽  
Lena Holmberg ◽  
Per Henrik Vincent ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Stem Cells ◽  
Progenitor Cells ◽  
Rat Model ◽  
Precursor Cells ◽  
Thin Layers ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Cord Injury ◽  
Neural Stem Progenitor Cells

AbstractPosttraumatic syringomyelia (PTS) is a serious condition of progressive expansion of spinal cord cysts, affecting patients with spinal cord injury years after injury. To evaluate neural cell therapy to prevent cyst expansion and potentially replace lost neurons, we developed a rat model of PTS. We combined contusive trauma with subarachnoid injections of blood, causing tethering of the spinal cord to the surrounding vertebrae, resulting in chronically expanding cysts. The cysts were usually located rostral to the injury, extracanalicular, lined by astrocytes. T2*-weighted magnetic resonance imaging (MRI) showed hyperintense fluid-filled cysts but also hypointense signals from debris and iron-laden macrophages/microglia. Two types of human neural stem/progenitor cells—fetal neural precursor cells (hNPCs) and neuroepithelial-like stem cells (hNESCs) derived from induced pluripotent stem cells—were transplanted to PTS cysts. Cells transplanted into cysts 10 weeks after injury survived at least 10 weeks, migrated into the surrounding parenchyma, but did not differentiate during this period. The cysts were partially obliterated by the cells, and cyst walls often merged with thin layers of cells in between. Cyst volume measurements with MRI showed that the volumes continued to expand in sham-transplanted rats by 102%, while the cyst expansion was effectively prevented by hNPCs and hNESCs transplantation, reducing the cyst volumes by 18.8% and 46.8%, respectively. The volume reductions far exceeded the volume of the added human cells. Thus, in an animal model closely mimicking the clinical situation, we provide proof-of-principle that transplantation of human neural stem/progenitor cells can be used as treatment for PTS.

Transplantation of expanded neural precursor cells from the developing pig ventral mesencephalon in a rat model of Parkinson's disease

2003 ◽  
Vol 151 (2) ◽  
pp. 204-217 ◽  
Author(s):  
Richard J. E. Armstrong ◽  
Pamela Tyers ◽  
Meena Jain ◽  
Andrew Richards ◽  
Stephen B. Dunnett ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rat Model ◽  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Ventral Mesencephalon

EphA4 Regulates Hippocampal Neural Precursor Proliferation in the Adult Mouse Brain by d-Serine Modulation of N-Methyl-d-Aspartate Receptor Signaling

2018 ◽  
Vol 29 (10) ◽  
pp. 4381-4397 ◽  
Author(s):  
Jing Zhao ◽  
Chanel J Taylor ◽  
Estella A Newcombe ◽  
Mark D Spanevello ◽  
Imogen O’Keeffe ◽  
...  
Keyword(s):  
Mouse Brain ◽  
Adult Mouse ◽  
Precursor Cells ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Neural Precursor ◽  
Adult Mouse Brain ◽  
Precursor Activity

Abstract The hippocampal dentate gyrus (DG) is a major region of the adult rodent brain in which neurogenesis occurs throughout life. The EphA4 receptor, which regulates neurogenesis and boundary formation in the developing brain, is also expressed in the adult DG, but whether it regulates adult hippocampal neurogenesis is not known. Here, we show that, in the adult mouse brain, EphA4 inhibits hippocampal precursor cell proliferation but does not affect precursor differentiation or survival. Genetic deletion or pharmacological inhibition of EphA4 significantly increased hippocampal precursor proliferation in vivo and in vitro, by blocking EphA4 forward signaling. EphA4 was expressed by mature hippocampal DG neurons but not neural precursor cells, and an EphA4 antagonist, EphA4-Fc, did not activate clonal cultures of precursors until they were co-cultured with non-precursor cells, indicating an indirect effect of EphA4 on the regulation of precursor activity. Supplementation with d-serine blocked the increased precursor proliferation induced by EphA4 inhibition, whereas blocking the interaction between d-serine and N-methyl-d-aspartate receptors (NMDARs) promoted precursor activity, even at the clonal level. Collectively, these findings demonstrate that EphA4 indirectly regulates adult hippocampal precursor proliferation and thus plays a role in neurogenesis via d-serine-regulated NMDAR signaling.

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