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Kihi-to, a herbal traditional medicine, improves Abeta(25–35)-induced memory impairment and losses of neurites and synapses
Chihiro Tohda, Rie Naito, Eri Joyashiki
BMC Complementary and Alternative Medicine , 2008, DOI: 10.1186/1472-6882-8-49
Abstract: Effects of Kihi-to, a traditional Japanese-Chinese traditional medicine, on memory deficits and losses of neurites and synapses were examined using Alzheimer's disease model mice. Improvements of Aβ(25–35)-induced neuritic atrophy by Kihi-to and the mechanism were investigated in cultured cortical neurons.Administration of Kihi-to for consecutive 3 days resulted in marked improvements of Aβ(25–35)-induced impairments in memory acquisition, memory retention, and object recognition memory in mice. Immunohistochemical comparisons suggested that Kihi-to attenuated neuritic, synaptic and myelin losses in the cerebral cortex, hippocampus and striatum. Kihi-to also attenuated the calpain increase in the cerebral cortex and hippocampus. When Kihi-to was added to cells 4 days after Aβ(25–35) treatment, axonal and dendritic outgrowths in cultured cortical neurons were restored as demonstrated by extended lengths of phosphorylated neurofilament-H (P-NF-H) and microtubule-associated protein (MAP)2-positive neurites. Aβ(25–35)-induced cell death in cortical culture was also markedly inhibited by Kihi-to. Since NF-H, MAP2 and myelin basic protein (MBP) are substrates of calpain, and calpain is known to be involved in Aβ-induced axonal atrophy, expression levels of calpain and calpastatin were measured. Treatment with Kihi-to inhibited the Aβ(25–35)-evoked increase in the calpain level and decrease in the calpastatin level. In addition, Kihi-to inhibited Aβ(25–35)-induced calcium entry.In conclusion Kihi-to clearly improved the memory impairment and losses of neurites and synapses.Neuronal death, neuritic atrophy, and loss of synapses underlie the pathogenesis of Alzheimer's [1-3]. However, neurons with atrophic neurites may remain viable and have the potential to remodel, even when neuronal death has occurred in other parts of the brain. We previously hypothesized that achievement of recovery of brain function after the injury requires the reconstruction of neuronal networks, inc
Marked electrical synapses on AP neuron of the leech (Whitmania pigra)
Duanwen Shen,Li Wang,Renji Zhang
Chinese Science Bulletin , 1998, DOI: 10.1007/BF02883686
Abstract: An initial attempt reveals parameters of marked electric synapse on AP perceptive neuron of leech. The width of gap between marked AP and either neuro-or glio-process is 2–3 nm, the diameter of the hexagonal array of connexion is 8–9 nm with a central pole of 2–2.5 nm, the same as the structure of annular lamellar bodies internalized by AP-glia processes in the AP.
Coseeded Schwann cells myelinate neurites from differentiated neural stem cells in neurotrophin-3-loaded PLGA carriers
Xiong Y, Zhu JX, Fang ZY, Zeng CG, Zhang C, Qi GL, Li MH, Zhang W, Quan DP, Wan J
International Journal of Nanomedicine , 2012, DOI: http://dx.doi.org/10.2147/IJN.S30706
Abstract: seeded Schwann cells myelinate neurites from differentiated neural stem cells in neurotrophin-3-loaded PLGA carriers Original Research (2897) Total Article Views Authors: Xiong Y, Zhu JX, Fang ZY, Zeng CG, Zhang C, Qi GL, Li MH, Zhang W, Quan DP, Wan J Published Date April 2012 Volume 2012:7 Pages 1977 - 1989 DOI: http://dx.doi.org/10.2147/IJN.S30706 Received: 09 February 2012 Accepted: 09 March 2012 Published: 17 April 2012 Yi Xiong1,*, Ji-Xiang Zhu2,*, Zheng-Yu Fang1, Cheng-Guang Zeng2, Chao Zhang1, Guo-Long Qi3, Man-Hui Li1, Wei Zhang1, Da-Ping Quan2, Jun Wan1,4 1Biomedical Research Institute, Shenzhen-PKU-HKUST Medical Center, Shenzhen, 2DSAPM Lab, PCFM Lab, Institute of Polymer Science, School of Chemistry and Chemical Engineering, Sun Yat-sen University, Guangzhou, 3Department of Medical Information, Medical Collage of Jinan University, Guangzhou, 4Division of Life Science, the Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong, People's Republic of China *These authors contributed equally to this manuscript Abstract: Biomaterials and neurotrophic factors represent promising guidance for neural repair. In this study, we combined poly-(lactic acid-co-glycolic acid) (PLGA) conduits and neurotrophin-3 (NT-3) to generate NT-3-loaded PLGA carriers in vitro. Bioactive NT-3 was released stably and constantly from PLGA conduits for up to 4 weeks. Neural stem cells (NSCs) and Schwann cells (SCs) were coseeded into an NT-releasing scaffold system and cultured for 14 days. Immunoreactivity against Map2 showed that most of the grafted cells (>80%) were differentiated toward neurons. Double-immunostaining for synaptogenesis and myelination revealed the formation of synaptic structures and myelin sheaths in the coculture, which was also observed under electron microscope. Furthermore, under depolarizing conditions, these synapses were excitable and capable of releasing synaptic vesicles labeled with FM1-43 or FM4-64. Taken together, coseeding NSCs and SCs into NT-3-loaded PLGA carriers increased the differentiation of NSCs into neurons, developed synaptic connections, exhibited synaptic activities, and myelination of neurites by the accompanying SCs. These results provide an experimental basis that supports transplantation of functional neural construction in spinal cord injury.
Pro-inflammatory cytokine; tumor-necrosis factor-alpha (TNF-α) inhibits astrocytic support of neuronal survival and neurites outgrowth  [PDF]
Ebtesam M. Abd-El-Basse
Advances in Bioscience and Biotechnology (ABB) , 2013, DOI: 10.4236/abb.2013.48A2010
Abstract:

Reactive astrogliosis has been implicated in the failure of axonal regeneration in adult mammalian Central Nervous System (CNS). It is our hypothesis that inflammatory cytokines act upon astrocytes to alter their biochemical and physical properties, which may in turn be responsible for the failure of neuronal regeneration. We have therefore examined the effect of tumor-necrosis factor-alpha (TNF-α) on the ability of astrocytes to support the survival of the cortical neurons and the growth of the neurites. Mouse astrocytes and cortical neuronal cultures were prepared. It was observed that when neurons were cultured in absence of astrocytes only a few of them grew and survived only for 5-6 days. These neurons had small cell bodies and few, short neurites. However, when the same numbers of neurons were cultured on the top of astrocytes, more neurons grew and survived up to 16-18 days. They had bigger cell bodies and many long branched neurites that formed anestamosing networks. The neurons then coalesced and the neurites formed thick bundles. When the same numbers of neurons were grown on the top of astrocytes pre-treated with TNF-α, few neurons survived up to 13 days. The neurites of the survived neurons were shorter than neurites of neurons grown on normal astrocytes and did not form bundles. In addition, TNF-α stimulated the expression of glial fibrillary acidic protein (GFAP) by astrocytes. These results support that the pro-inflammatory cytokine, TNF-α modulates the gliosis and that the astrocytic cell supports neuronal survival and neurite outgrowth.

Effect of Interleukin-1Beta (IL-1β) on the Cortical Neurons Survival and Neurites Outgrowth  [PDF]
Ebtesam M. Abd-El-Basset
Advances in Bioscience and Biotechnology (ABB) , 2016, DOI: 10.4236/abb.2016.71004
Abstract: Insults to the brain are known to cause a myriad of downstream effects, including the release of cytokines by astrocytes and resultant reactive gliosis. The author has examined effect of cytokine IL-1β on the survival of cortical neurons using mouse astrocyte-neuron co-culture. Five groups were used. These were neurons alone (Group 1), neurons with added IL-1β (Group 2), neurons co-cultured with astrocytes (Group 3), neurons co-cultured with astrocytes that was pre-treated with IL-1β before co-culture (Group 4) and neurons co-cultured with astrocytes and IL-1β added (post-treated) (Group 5). In Group 1 only a few neurons grew and survived only for 5-6 days. In Group 2, it was observed that more neurons survived up to 11 days. Moreover, in Group 3, more neurons grew and survived up to 16-18 days. They had large cell bodies and many long neurites that formed anastomosing networks. In Group 4, few neurons survived up to 13 days, whereas in Group 5, the growth of neurons were affected but to a much lesser extent than Group 4 and survived up to 15 days. In addition, it was found that IL-1β stimulated the expression of glial fibrillary acidic protein (GFAP) by astrocytes. This study indicates that IL-1β affects the survival of cortical neurons and modulates the astrocytic support to neuronal survival and neurites outgrowth by acting directly on the astrocytes.
Both Pre- and Postsynaptic Activity of Nsf Prevents Degeneration of Hair-Cell Synapses  [PDF]
Weike Mo, Teresa Nicolson
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0027146
Abstract: Vesicle fusion contributes to the maintenance of synapses in the nervous system by mediating synaptic transmission, release of neurotrophic factors, and trafficking of membrane receptors. N-ethylmaleimide-sensitive factor (NSF) is indispensible for dissociation of the SNARE-complex following vesicle fusion. Although NSF function has been characterized extensively in vitro, the in vivo role of NSF in vertebrate synaptogenesis is relatively unexplored. Zebrafish possess two nsf genes, nsf and nsfb. Here, we examine the function of either Nsf or Nsfb in the pre- and postsynaptic cells of the zebrafish lateral line organ and demonstrate that Nsf, but not Nsfb, is required for maintenance of afferent synapses in hair cells. In addition to peripheral defects in nsf mutants, neurodegeneration of glutamatergic synapses in the central nervous system also occurs in the absence of Nsf function. Expression of an nsf transgene in a null background indicates that stabilization of synapses requires Nsf function in both hair cells and afferent neurons. To identify potential targets of Nsf-mediated fusion, we examined the expression of genes implicated in stabilizing synapses and found that transcripts for multiple genes including brain-derived neurotrophic factor (bdnf) were significantly reduced in nsf mutants. With regard to trafficking of BDNF, we observed a striking accumulation of BDNF in the neurites of nsf mutant afferent neurons. In addition, injection of recombinant BDNF protein partially rescued the degeneration of afferent synapses in nsf mutants. These results establish a role for Nsf in the maintenance of synaptic contacts between hair cells and afferent neurons, mediated in part via the secretion of trophic signaling factors.
Convergence of Synapses, Endosomes, and Prions in the Biology of Neurodegenerative Diseases  [PDF]
Gunnar K. Gouras
International Journal of Cell Biology , 2013, DOI: 10.1155/2013/141083
Abstract: Age-related misfolding and aggregation of disease-linked proteins in selective brain regions is a characteristic of neurodegenerative diseases. Although neuropathological aggregates that characterize these various diseases are found at sites other than synapses, increasing evidence supports the idea that synapses are where the pathogenesis begins. Understanding these diseases is hampered by our lack of knowledge of what the normal functions of these proteins are and how they are affected by aging. Evidence has supported the idea that neurodegenerative disease-linked proteins have a common propensity for prion protein-like cell-to-cell propagation. However, it is not thought that the prion-like quality of these proteins/peptides that allows their cell-to-cell transmission implies a role for human-to-human spread in common age-related neurodegenerative diseases. It will be important to better understand the molecular and cellular mechanisms governing the role of these aggregating proteins in neural function, especially at synapses, how their propagation occurs and how pathogenesis is promoted by aging. 1. Synapses The brain is particularly vulnerable to degenerative diseases of ageing. Aberrant aggregation of proteins/peptides is the common theme among these diseases. Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the most common age-related neurodegenerative diseases, while other less common, albeit devastating, neurodegenerative diseases include Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS), prion diseases, and frontotemporal dementia (FTD). Although the specific protein aggregates and selective cellular vulnerabilities differ, shared disease mechanisms are increasingly apparent among neurodegenerative diseases and next to aberrant protein aggregation also include anatomically selective cell-to-cell propagation. Major themes of research on these diseases have included therapeutic neurotransmitter replacement, most successful with dopamine for PD, elucidating the biology of aberrant protein misfolding, and trying to understand how ageing promotes the development of these diseases. More recently, synapses have moved more to the center of research on these diseases [1, 2]. Neurites (axons and dendrites) and synapses are a unique feature of neurons and play fundamental roles in brain function. Furthermore, the aggregation-prone proteins linked pathologically and genetically to neurodegenerative diseases are normally present particularly at synapses. For example, the PD-linked protein -synuclein is known to normally reside
Microglia Actively Regulate the Number of Functional Synapses  [PDF]
Kyungmin Ji, Gulcan Akgul, Lonnie P. Wollmuth, Stella E. Tsirka
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056293
Abstract: Microglia are the immunocompetent cells of the central nervous system. In the physiological setting, their highly motile processes continually survey the local brain parenchyma and transiently contact synaptic elements. Although recent work has shown that the interaction of microglia with synapses contributes to synaptic remodeling during development, the role of microglia in synaptic physiology is just starting to get explored. To assess this question, we employed an electrophysiological approach using two methods to manipulate microglia in culture: organotypic hippocampal brain slices in which microglia were depleted using clodronate liposomes, and cultured hippocampal neurons to which microglia were added. We show here that the frequency of excitatory postsynaptic current increases in microglia-depleted brain slices, consistent with a higher synaptic density, and that this enhancement ensures from the loss of microglia since it is reversed when the microglia are replenished. Conversely, the addition of microglia to neuronal cultures decreases synaptic activity and reduces the density of synapses, spine numbers, surface expression of AMPA receptor (GluA1), and levels of synaptic adhesion molecules. Taken together, our findings demonstrate that non-activated microglia acutely modulate synaptic activity by regulating the number of functional synapses in the central nervous system.
Presenilin/γ-Secretase Regulates Neurexin Processing at Synapses  [PDF]
Carlos A. Saura,Emilia Servián-Morilla,Francisco G. Scholl
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0019430
Abstract: Neurexins are a large family of neuronal plasma membrane proteins, which function as trans-synaptic receptors during synaptic differentiation. The binding of presynaptic neurexins to postsynaptic partners, such as neuroligins, has been proposed to participate in a signaling pathway that regulates synapse formation/stabilization. The identification of mutations in neurexin genes associated with autism and mental retardation suggests that dysfunction of neurexins may underlie synaptic defects associated with brain disorders. However, the mechanisms that regulate neurexin function at synapses are still unclear. Here, we show that neurexins are proteolytically processed by presenilins (PS), the catalytic components of the γ-secretase complex that mediates the intramembraneous cleavage of several type I membrane proteins. Inhibition of PS/γ-secretase by using pharmacological and genetic approaches induces a drastic accumulation of neurexin C-terminal fragments (CTFs) in cultured rat hippocampal neurons and mouse brain. Neurexin-CTFs accumulate mainly at the presynaptic terminals of PS conditional double knockout (PS cDKO) mice lacking both PS genes in glutamatergic neurons of the forebrain. The fact that loss of PS function enhances neurexin accumulation at glutamatergic terminals mediated by neuroligin-1 suggests that PS regulate the processing of neurexins at glutamatergic synapses. Interestingly, presenilin 1 (PS1) is recruited to glutamatergic terminals mediated by neuroligin-1, thus concentrating PS1 at terminals containing β-neurexins. Furthermore, familial Alzheimer's disease (FAD)-linked PS1 mutations differentially affect β-neurexin-1 processing. Expression of PS1 M146L and PS1 H163R mutants in PS?/? cells rescues the processing of β-neurexin-1, whereas PS1 C410Y and PS1 ΔE9 fail to rescue the processing defect. These results suggest that PS regulate the synaptic function and processing of neurexins at glutamatergic synapses, and that impaired neurexin processing by PS may play a role in FAD.
Frames in the odd Leech lattice  [PDF]
Tsuyoshi Miezaki
Mathematics , 2012,
Abstract: In this paper, we show that there is a frame of norm k in the odd Leech lattice for every k\ge 3.
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