1.Neurourological Application of Neurogenesis and Inflammation and Pain Mechanisms of Rocuronium Bromide.
International Neurourology Journal 2016;20(4):274-275
No abstract available.
Inflammation*
;
Neurogenesis*
2.Adult Neurological Handicap: New Insight from Neurogenesis.
International Neurourology Journal 2012;16(2):55-56
No abstract available.
Adult
;
Humans
;
Neurogenesis
4.Biological effects of blood–brain barrier disruption using a focused ultrasound.
Mun HAN ; Yongki HUR ; Jieun HWANG ; Juyoung PARK
Biomedical Engineering Letters 2017;7(2):115-120
With focused ultrasound (FUS) and microbubbles, BBB can be transiently disrupted with a localized and non-invasive approach. BBB disruption induced by FUS has made progressions to move forward on delivery of therapeutic agents into a brain in a specific area of brain for better treatment of neurological diseases. In addition to be used as an improvement of drug delivery, BBB disruption has been found to induce biological effects such as a clearance of protein aggregation which cause Alzheimer's disease, regulation of proteins which facilitate drug uptake, and modulation of neuronal function and neurogenesis. In this review, we discuss overview about the principles of BBB opening with FUS and milestones in these biological effects of FUS-induced BBB disruption.
Alzheimer Disease
;
Brain
;
Microbubbles
;
Neurogenesis
;
Neurons
;
Ultrasonography*
5.Unlocking the Neurogenic Potential of Mammalian Müller Glia.
International Journal of Stem Cells 2016;9(2):169-175
Müller glia (MG) are the primary support cells in the vertebrate retina, regulating homeostasis in one of the most metabolically active tissues. In lower vertebrates such as fish, they respond to injury by proliferating and reprogramming to regenerate retinal neurons. In mammals, MG may also react to injury by proliferating, but they fail to initiate regeneration. The barriers to regeneration could be intrinsic to mammalian MG or the function of the niche that cannot support the MG reprogramming required for lineage conversion or both. Understanding these mechanisms in light of those being discovered in fish may lead to the formulation of strategies to unlock the neurogenic potential of MG and restore regeneration in the mammalian retina.
Homeostasis
;
Mammals
;
Neurogenesis
;
Neuroglia*
;
Regeneration
;
Retina
;
Retinal Neurons
;
Vertebrates
6.The Effects of Repeated Restraint Stress on the Synaptic Plasticity in the Inner Molecular Layer of Mouse Dentate Gyrus.
Mi Sook YOON ; Minho MOON ; Joo Won JEONG ; Junghye KIM ; Heekyung AHN ; Youngbuhm HUH ; Chan PARK
Korean Journal of Physical Anthropology 2006;19(4):325-337
Stress induces degeneration of brain structures and functions. Particularly, hippocampus is sensitive to stressful stimulations. In the present study, the change of synaptic related molecules in the mouse dentate gyrus was examined with immunohistochemistry after restraint stress. We subjected mice to restraint stress for 6 h per day for 4 days. As a result, the number of Ki-67, a marker for proliferation, and doublecortin (DCX), a marker for neurogenesis, immunoreactive cells was decreased in the stress group. On the other hand, the intensity of calbindinD-28k, a marker of pre-existing granule cells, immunoreactivity was increased in the granule cell layer after 4 days restraint stress. As well as, the immunoreactivity of synaptic related molecules, postsynaptic density-95 (PSD-95), growth association protein-43 (GAP-43) and beta-NADPH-d reactivity were increased in the inner molecular layer of dentate gyrus after 4 days restraint stress. In conclusion, this study shows that repeated restraint stress suppresses neurogenesis in dentate gyrus and strengthens synaptic plasticity of existing granule cells.
Animals
;
Brain
;
Dentate Gyrus*
;
Hand
;
Hippocampus
;
Immunohistochemistry
;
Mice*
;
Neurogenesis
;
Plastics*
7.Visualization analysis of traditional Chinese medicine for neurogenesis research based on CiteSpace.
Li-Hua XIE ; Xiao-Yuan LIN ; Xin LI ; Yan SHANG ; Jin-Ru XIE ; Guo-Heng HU
China Journal of Chinese Materia Medica 2021;46(17):4555-4562
To analyze the research hotspots and trends of traditional Chinese medicine(TCM) for neurogenesis with use of CiteSpace 5.7.R3 software. The bibliometrics analysis on the literatures of TCM for neurogenesis from 1987 to 2020 included in the CNKI database was conducted to visualize the number of papers, authors, institutions and keywords. Totally 736 literatures were included and the volume of annual publications showed an upward in volatility. At present, several stable research teams have been formed, which were represented by DING Fei, ZHOU Chong-jian and ZHOU Yong-hong, but the cooperation was not close among the teams. According to the analysis of research institutions, Institute of Diagnostics of Hunan University of Chinese Medicine and Acupuncture Research Center of Tianjin University of Traditional Chinese Medicine produced largest number of literatures. The cooperation among institutions, with universities of TCM and affiliated hospitals as the main research force, was characterized by dominant cooperation among regional institutions and less cross-regional cooperation. Keywords analysis showed that in the field of TCM for neurogenesis, a lot of studies mainly focused on the disease field, treatment and medication, TCM therapy and molecular mechanism. The research on TCM therapy and molecular mechanism for neurogenesis of central nervous system will be the research hotspots in future.
Acupuncture Therapy
;
Bibliometrics
;
Databases, Factual
;
Medicine, Chinese Traditional
;
Neurogenesis
8.Reprogramming Glial Cells into Functional Neurons for Neuro-regeneration: Challenges and Promise.
Fengchao WANG ; Leping CHENG ; Xiaohui ZHANG
Neuroscience Bulletin 2021;37(11):1625-1636
The capacity for neurogenesis in the adult mammalian brain is extremely limited and highly restricted to a few regions, which greatly hampers neuronal regeneration and functional restoration after neuronal loss caused by injury or disease. Meanwhile, transplantation of exogenous neuronal stem cells into the brain encounters several serious issues including immune rejection and the risk of tumorigenesis. Recent discoveries of direct reprogramming of endogenous glial cells into functional neurons have provided new opportunities for adult neuro-regeneration. Here, we extensively review the experimental findings of the direct conversion of glial cells to neurons in vitro and in vivo and discuss the remaining issues and challenges related to the glial subtypes and the specificity and efficiency of direct cell-reprograming, as well as the influence of the microenvironment. Although in situ glial cell reprogramming offers great potential for neuronal repair in the injured or diseased brain, it still needs a large amount of research to pave the way to therapeutic application.
Animals
;
Cellular Reprogramming
;
Nerve Regeneration
;
Neurogenesis
;
Neuroglia
;
Neurons
9.Postnatal changes in glucose transporter 3 expression in the dentate gyrus of the C57BL/6 mouse model.
Hyo Young JUNG ; Hee Sun YIM ; Dae Young YOO ; Jong Whi KIM ; Jin Young CHUNG ; Je Kyung SEONG ; Yeo Sung YOON ; Dae Won KIM ; In Koo HWANG
Laboratory Animal Research 2016;32(1):1-7
In this study, we observed the ontogenetic changes in glucose transporter 3 (GLUT3) immunoreactivity, a major neuronal GLUT, in the dentate gyrus of mouse brains at various ages: postnatal day (P) 1, 7, 14, 28, and 56. At P1, cresyl violet staining showed abundant neurons in the dentate gyrus, whereas the granule cell layer was ill-defined. At P7, the granule cell layer was observed, and cresyl violet-positive cells were dispersed throughout the polymorphic layer. At P14, the granule cell layer was well-defined, and cresyl violet positive cells were detected abundantly in the polymorphic layer. At P28 and P56, cresyl violet-positive cells were observed in the granule cell layer, as well as in the polymorphic layer. At P1, GLUT3 immunoreactivity was detected in the dentate gyrus. At P7, GLUT3 immunoreactive cells were scattered in the polymorphic and molecular layer. However, at P14, GLUT3 immunoreactivity was observed in the polymorphic layer as well as subgranular zone of the dentate gyrus. At P28, GLUT3 immunoreactivity was detected in the polymorphic layer of the dentate gyrus. At P56, GLUT3 immunoreactivity was observed predominantly in the subgranular zone of the dentate gyrus. GLUT3 immunoreactive cells were mainly colocalized with doublecortin, which is a marker for differentiated neuroblasts, in the polymorphic layer and subgranular zone of dentate gyrus at P14 and P56. These results suggest that the expression of GLUT3 is closely associated with postnatal development of the dentate gyrus and adult neurogenesis.
Adult
;
Animals
;
Brain
;
Dentate Gyrus*
;
Glucose Transport Proteins, Facilitative*
;
Glucose*
;
Humans
;
Mice*
;
Neurogenesis
;
Neurons
;
Viola
10.The Role of the PI3K Pathway in the Regeneration of the Damaged Brain by Neural Stem Cells after Cerebral Infarction.
Journal of Clinical Neurology 2015;11(4):297-304
Neurologic deficits resulting from stroke remain largely intractable, which has prompted thousands of studies aimed at developing methods for treating these neurologic sequelae. Endogenous neurogenesis is also known to occur after brain damage, including that due to cerebral infarction. Focusing on this process may provide a solution for treating neurologic deficits caused by cerebral infarction. The phosphatidylinositol-3-kinase (PI3K) pathway is known to play important roles in cell survival, and many studies have focused on use of the PI3K pathway to treat brain injury after stroke. Furthermore, since the PI3K pathway may also play key roles in the physiology of neural stem cells (NSCs), eliciting the appropriate activation of the PI3K pathway in NSCs may help to improve the sequelae of cerebral infarction. This review describes the PI3K pathway, its roles in the brain and NSCs after cerebral infarction, and the therapeutic possibility of activating the pathway to improve neurologic deficits after cerebral infarction.
Brain Injuries
;
Brain*
;
Cell Survival
;
Cerebral Infarction*
;
Neural Stem Cells*
;
Neurogenesis
;
Neurologic Manifestations
;
Physiology
;
Regeneration*
;
Stroke