scholarly journals Function of neural stem cells in ischemic brain repair processes

2016 ◽  
Vol 36 (12) ◽  
pp. 2034-2043 ◽  
Author(s):  
Ruilan Zhang ◽  
Zhenggang Zhang ◽  
Michael Chopp

Hypoxic/ischemic injury is the single most important cause of disabilities in infants, while stroke remains a leading cause of morbidity in children and adults around the world. The injured brain has limited repair capacity, and thereby only modest improvement of neurological function is evident post injury. In rodents, embryonic neural stem cells in the ventricular zone generate cortical neurons, and adult neural stem cells in the ventricular–subventricular zone of the lateral ventricle produce new neurons through animal life. In addition to generation of new neurons, neural stem cells contribute to oligodendrogenesis. Neurogenesis and oligodendrogenesis are essential for repair of injured brain. Much progress has been made in preclinical studies on elucidating the cellular and molecular mechanisms that control and coordinate neurogenesis and oligodendrogenesis in perinatal hypoxic/ischemic injury and the adult ischemic brain. This article will review these findings with a focus on the ventricular–subventricular zone neurogenic niche and discuss potential applications to facilitate endogenous neurogenesis and thereby to improve neurological function post perinatal hypoxic/ischemic injury and stroke.

2014 ◽  
Vol 75 (5) ◽  
pp. 603-611 ◽  
Author(s):  
Stephen Ashwal ◽  
Nirmalya Ghosh ◽  
Christine I. Turenius ◽  
Melissa Dulcich ◽  
Christopher M. Denham ◽  
...  

2011 ◽  
Vol 89 (8) ◽  
pp. 1185-1193 ◽  
Author(s):  
Gadi Turgeman ◽  
Adi Pinkas ◽  
Theodore A. Slotkin ◽  
Matanel Tfilin ◽  
Rachel Langford ◽  
...  

2017 ◽  
Vol 222 (6) ◽  
pp. 2855-2876 ◽  
Author(s):  
Valentina Mastrorilli ◽  
Chiara Scopa ◽  
Daniele Saraulli ◽  
Marco Costanzi ◽  
Raffaella Scardigli ◽  
...  

2005 ◽  
Vol 58 (3) ◽  
pp. 600-606 ◽  
Author(s):  
Jennifer Ong ◽  
Jennifer M Plane ◽  
Jack M Parent ◽  
Faye S Silverstein

2020 ◽  
Author(s):  
Huanhuan Sha ◽  
Peipei Peng ◽  
Bing Li ◽  
Guohua Wei ◽  
Juan Wang ◽  
...  

Abstract Background: Recently, the number of neonatal patients receiving surgery under general anesthesia has increased. Ketamine disrupts the proliferation and differentiation of developing neural stem cells (NSCs). Therefore, the safe use of ketamine in pediatric anesthesia has been an issue of increasing concern among anesthesiologists and the children’s parents. Dexmedetomidine (DEX) is widely used in sedation, as an antianxiety agent and for analgesia. DEX has recently been shown to provide neuroprotection against anesthetic-induced neurotoxicity in the developing brain. The aim of this in vivo study was to investigate whether DEX exerted neuroprotective effects on the proliferation and differentiation of NSCs in the subventricular zone (SVZ) following neonatal ketamine exposure. Methods: Postnatal day 7 (PND-7) male Sprague-Dawley rats were equally divided into the following 5 groups: Control group (n=8), Ketamine group (n=8), 1 μg/kg DEX+Ketamine group (n=8), 5 μg/kg DEX+Ketamine group (n=8) and 10 μg/kg DEX+Ketamine group (n=8). The proliferation and differentiation of NSCs in the SVZ were assessed using immunostaining with BrdU incorporation. The levels of Nestin and β-tubulin III in the SVZ were measured using Western blot analyses. Apoptosis was assessed by detecting the levels of the cleaved caspase-3 protein using Western blotting. Results: Neonatal ketamine exposure significantly inhibited NSC proliferation and astrocytic differentiation in the SVZ, and neuronal differentiation was markedly increased. Furthermore, pretreatment with moderate (5 μg/kg) or high doses (10 μg/kg) of DEX reversed the ketamine-induced disturbances in the proliferation and differentiation of NSCs. Meanwhile, neonatal ketamine exposure significantly decreased the expression of Nestin and increased the expression of β-tubulin III in the SVZ compared with the Control group. Treatment with 10 μg/kg DEX notably reversed the ketamine-induced changes in the levels of Nestin and β-tubulin III. In addition, a pretreatment with 10 μg/kg DEX before ketamine anesthesia prevented apoptosis in the SVZ induced by neonatal ketamine exposure. Conclusions: Based on our findings, DEX may exert neuroprotective effects on the proliferation and differentiation of NSCs in the SVZ of neonatal rats in a repeated ketamine anesthesia model.


ASN NEURO ◽  
2013 ◽  
Vol 5 (3) ◽  
pp. AN20120032 ◽  
Author(s):  
Dhivyaa Alagappan ◽  
Murugabaskar Balan ◽  
Yuhui Jiang ◽  
Rachel B. Cohen ◽  
Sergei V. Kotenko ◽  
...  

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