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[PMID]: 29524470
[Au] Autor:Zheng Y; Huang C; Liu F; Lin H; Niu Y; Yang X; Zhang Z
[Ad] Address:Department of Anatomy, Institute of Biomedical Engineering, Second Military Medical University, Shanghai 200433, China.
[Ti] Title:Reactivation of denervated Schwann cells by neurons induced from bone marrow-derived mesenchymal stem cells.
[So] Source:Brain Res Bull;, 2018 Mar 07.
[Is] ISSN:1873-2747
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The use of neurons induced from stem cells has been introduced as an effective strategy for promoting peripheral nerve regeneration (PNR). The evolution and role of native denervated Schwann cells (SCs) were often ignored when exploring the mechanisms underlying neural transplantation therapy for PNR. The aim of this study was to understand if following injury, native denervated SCs could be reactivated by transplanting of neurons induced from bone marrow-derived mesenchymal stem cells (NI-BMSCs) to promote PNR. We co-cultured denervated SCs with NI-BMSCs in vitro, tested the proliferation of denervated SCs, and measured the expression and secretion of neurotrophic factors and neural adhesion molecules of the denervated SCs. Concurrently, 48 adult male Sprague-Dawley rats were randomly divided into 4 even groups of 12 rats each: normal group, phosphate-buffered saline (PBS) injection group, BMSCs transplantation group and NI-BMSCs transplantation group. PBS injection and cells transplantation were performed 4 weeks post-injury. After 4 weeks of NI-BMSCs transplantation, the survival of seeded NI-BMSCs was examined, proliferation and ultrastructure of native denervated SCs were detected, and myelination, axonal regeneration and the sciatic functional index measurements were also determinated. Our results demonstrated that NI-BMSCs reactivated denervated SCs both in vitro and in vivo and promoted sciatic nerve regeneration.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 106032 MEDLINE  
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[PMID]: 29524419
[Au] Autor:Eguchi N; Sora I; Muguruma K
[Ad] Address:Laboratory for Cell Asymmetry, RIKEN Center for Developmental Biology, Kobe, 650-0047, Japan; Department of Psychiatry, Kobe University Graduate School of Medicine, Kobe, 650-0017, Japan.
[Ti] Title:Self-organizing cortex generated from human iPSCs with combination of FGF2 and ambient oxygen.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Human brain development has generally been studied through the analysis of postmortem tissues because of limited access to fetal brain tissues. This approach, however, only provides information from the perspective of long-term development. To investigate the pathophysiology of neurodevelopmental disorders, it is necessary to understand the detailed mechanisms of human brain development. Recent advances in pluripotent stem cell (PSC) technologies enable us to establish in vitro brain models from human induced PSCs (hiPSCs), which can be used to examine the pathophysiological mechanisms of neurodevelopmental disorders. We previously demonstrated that self-organized cerebral tissues can be generated from human PSCs in a three-dimensional (3D) culture system. Here, we describe the cerebral tissues differentiated from hiPSCs in a further-optimized 3D culture. We found that treatment with FGF2 is helpful to form iPSC aggregates with efficiency. Neuroepithelial structures spontaneously formed with apico-basal polarity in the aggregates expressing forebrain marker FOXG1. The neuroepithelium self-forms a multilayered structure including progenitor zones (ventricular and subventricular zones) and neuronal zone (cortical plate). Furthermore, with the same level of oxygen (O ) as in ambient air (20% O ), we found that self-formation of cortical structures lasted for 70 days in culture. Thus, our optimized 3D culture for the generation of cortical structure from hiPSCs is a simple yet effective method.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 106032 MEDLINE  
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[PMID]: 29486219
[Au] Autor:Parsons-White AB; Spitzer N
[Ad] Address:Department of Biological Sciences, Marshall University, 1 John Marshall Dr, Huntington, WV 25755, USA.
[Ti] Title:Environmentally relevant manganese overexposure alters neural cell morphology and differentiation in vitro.
[So] Source:Toxicol In Vitro;50:22-28, 2018 Mar 02.
[Is] ISSN:1879-3177
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Manganese (Mn) is a trace metal and micronutrient that is necessary for neurological function. Because of its ability to cross the blood brain barrier, excessive amounts of Mn are neurotoxic and can lead to a neurological disorder, manganism. Environmental overexposure to Mn correlates with impaired cognitive development in children. Though symptoms of manganism and overexposure are well defined, the changes in cellular mechanisms underlying these symptoms are not fully understood. We used cultured adult neural stem cells (NSCs) from young adult rats as an accessible model to investigate the effect of Mn on cellular mechanisms underlying neural differentiation. Concentrations of Mn below current EPA limits caused a dose- and time-dependent collapse of neurites and restructuring of cellular morphology. This effect was confirmed in B35 neuroblastoma cells. These findings indicate that Mn alters cytoskeleton dynamics during differentiation. In addition, Mn overexposure caused downregulation of DCX, a neuronal migration marker, and GFAP, a neural stem cell and astrocyte marker, in NSCs. We conclude that environmentally relevant concentrations of Mn impair cytoskeletal structure and morphology, and may impair differentiation in NSCs. These effects of Mn overexposure on brain cell function could underlie manganism and neurocognitive and developmental defects associated with environmental Mn overexposure.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 106032 MEDLINE  
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[PMID]: 29478844
[Au] Autor:Peruzzotti-Jametti L; Bernstock JD; Vicario N; Costa ASH; Kwok CK; Leonardi T; Booty LM; Bicci I; Balzarotti B; Volpe G; Mallucci G; Manferrari G; Donegà M; Iraci N; Braga A; Hallenbeck JM; Murphy MP; Edenhofer F; Frezza C; Pluchino S
[Ad] Address:Department of Clinical Neurosciences and NIHR Biomedical Research Centre, University of Cambridge, Cambridge, UK. Electronic address: lp429@cam.ac.uk.
[Ti] Title:Macrophage-Derived Extracellular Succinate Licenses Neural Stem Cells to Suppress Chronic Neuroinflammation.
[So] Source:Cell Stem Cell;22(3):355-368.e13, 2018 Mar 01.
[Is] ISSN:1875-9777
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Neural stem cell (NSC) transplantation can influence immune responses and suppress inflammation in the CNS. Metabolites, such as succinate, modulate the phenotype and function of immune cells, but whether and how NSCs are also activated by such immunometabolites to control immunoreactivity and inflammatory responses is unclear. Here, we show that transplanted somatic and directly induced NSCs ameliorate chronic CNS inflammation by reducing succinate levels in the cerebrospinal fluid, thereby decreasing mononuclear phagocyte (MP) infiltration and secondary CNS damage. Inflammatory MPs release succinate, which activates succinate receptor 1 (SUCNR1)/GPR91 on NSCs, leading them to secrete prostaglandin E2 and scavenge extracellular succinate with consequential anti-inflammatory effects. Thus, our work reveals an unexpected role for the succinate-SUCNR1 axis in somatic and directly induced NSCs, which controls the response of stem cells to inflammatory metabolic signals released by type 1 MPs in the chronically inflamed brain.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  5 / 106032 MEDLINE  
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[PMID]: 29471071
[Au] Autor:Gartner SN; Aidney F; Klockars A; Prosser C; Carpenter EA; Isgrove K; Levine AS; Olszewski PK
[Ad] Address:University of Waikato, Hamilton, New Zealand.
[Ti] Title:Intragastric preloads of l-tryptophan reduce ingestive behavior via oxytocinergic neural mechanisms in male mice.
[So] Source:Appetite;125:278-286, 2018 Feb 19.
[Is] ISSN:1095-8304
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Human and laboratory animal studies suggest that dietary supplementation of a free essential amino acid, l-tryptophan (TRP), reduces food intake. It is unclear whether an acute gastric preload of TRP decreases consumption and whether central mechanisms underlie TRP-driven hypophagia. We examined the effect of TRP administered via intragastric gavage on energy- and palatability-induced feeding in mice. We sought to identify central mechanisms through which TRP suppresses appetite. Effects of TRP on consumption of energy-dense and energy-dilute tastants were established in mice stimulated to eat by energy deprivation or palatability. A conditioned taste aversion (CTA) paradigm was used to assess whether hypophagia is unrelated to sickness. c-Fos immunohistochemistry was employed to detect TRP-induced activation of feeding-related brain sites and of oxytocin (OT) neurons, a crucial component of satiety circuits. Also, expression of OT mRNA was assessed with real-time PCR. The functional importance of OT in mediating TRP-driven hypophagia was substantiated by showing the ability of OT receptor blockade to abolish TRP-induced decrease in feeding. TRP reduced intake of energy-dense standard chow in deprived animals and energy-dense palatable chow in sated mice. Anorexigenic doses of TRP did not cause a CTA. TRP failed to affect intake of palatable yet calorie-dilute or noncaloric solutions (10% sucrose, 4.1% Intralipid or 0.1% saccharin) even for TRP doses that decreased water intake in thirsty mice. Fos analysis revealed that TRP increases activation of several key feeding-related brain areas, especially in the brain stem and hypothalamus. TRP activated hypothalamic OT neurons and increased OT mRNA levels, whereas pretreatment with an OT antagonist abolished TRP-driven hypophagia. We conclude that intragastric TRP decreases food and water intake, and TRP-induced hypophagia is partially mediated via central circuits that encompass OT.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 106032 MEDLINE  
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[PMID]: 29471003
[Au] Autor:Anand SK; Mondal AC
[Ad] Address:Laboratory of Cellular & Molecular Neurobiology, School of Life Sciences, Jawaharlal Nehru University, New Mehrauli Road, New Delhi, 110067, India.
[Ti] Title:TrkB receptor antagonism inhibits stab injury induced proliferative response in adult zebrafish (Danio rerio) brain.
[So] Source:Neurosci Lett;672:28-33, 2018 Feb 20.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:The Tropomyosin related kinase B (TrkB) receptor, is known to promote neuronal maturation, differentiation, maintenance and survival through its cognate ligands Brain derived neurotrophic factor (BDNF) and neurotrophin 4 (NT4). BDNF, NT4 and TrkB are highly conserved proteins among vertebrates. Although the role of TrkB during brain development is well established, its role in adult neurogenesis and brain regeneration awaits thorough investigation. In this study, we used the zebrafish stab wound injury model to determine whether the injury induced regeneration response in the telencephalon region is governed by TrkB or not. We induced stab wound injury in the mid-dorsal region of telencephalon of ANA-12 (selective TrkB antagonist) treated and non-treated zebrafish brain and examined the proliferation activity in selected brain regions using immunohistochemistry. We found that proliferation activity was significantly low in ANA-12 injected injured fishes as compared to vehicle control injured fishes. Other major findings of the study include the temporal pattern of proliferation activity after an injury and activation of adult neural stem cells (aNSCs) situated distantly apart from the injury site in the adult zebrafish brain.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 106032 MEDLINE  
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[PMID]: 29460030
[Au] Autor:Vogel KR; Ainslie GR; Walters DC; McConnell A; Dhamne SC; Rotenberg A; Roullet JB; Gibson KM
[Ad] Address:Department of Neuroscience, University of Wisconsin, Madison, WI, USA.
[Ti] Title:Succinic semialdehyde dehydrogenase deficiency, a disorder of GABA metabolism: an update on pharmacological and enzyme-replacement therapeutic strategies.
[So] Source:J Inherit Metab Dis;, 2018 Feb 19.
[Is] ISSN:1573-2665
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:We present an update to the status of research on succinic semialdehyde dehydrogenase (SSADH) deficiency (SSADHD), a rare disorder of GABA metabolism. This is an unusual disorder featuring the accumulation of both GABA and its neuromodulatory analog, gamma-hydroxybutyric acid (GHB), and recent studies have advanced the potential clinical application of NCS-382, a putative GHB receptor antagonist. Animal studies have provided proof-of-concept that enzyme replacement therapy could represent a long-term therapeutic option. The characterization of neuronal stem cells (NSCs) derived from aldehyde dehydrogenase 5a1 (aldh5a1 ) mice, the murine model of SSADHD, has highlighted NSC utility as an in vitro system in which to study therapeutics and associated toxicological properties. Gene expression analyses have revealed that transcripts encoding GABA receptors are down-regulated and may remain largely immature in aldh5a1 brain, characterized by excitatory as opposed to inhibitory outputs, the latter being the expected action in the mature central nervous system. This indicates that agents altering chloride channel activity may be therapeutically relevant in SSADHD. The most recent therapeutic prospects include mTOR (mechanistic target of rapamycin) inhibitors, drugs that have received attention with the elucidation of the effects of elevated GABA on autophagy. The outlook for novel therapeutic trials in SSADHD continues to improve.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1007/s10545-018-0153-8

  8 / 106032 MEDLINE  
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[PMID]: 29424769
[Au] Autor:Hellman N; Kuhn BL; Lannon EW; Payne MF; Sturycz CA; Palit S; Shadlow JO; Rhudy JL
[Ad] Address:Department of Psychology, The University of Tulsa, Tulsa OK.
[Ti] Title:Emotional Modulation of Pain and Spinal Nociception in Sexual Assault Survivors.
[So] Source:Psychosom Med;, 2018 Feb 09.
[Is] ISSN:1534-7796
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Sexual assault (SA) is associated with an increased risk for chronic pain and affective distress. Given that emotional processes modulate pain (e.g., negative emotions enhance pain, positive emotions inhibit pain), increased pain risk in SA survivors could stem from a disruption of emotional modulation processes. METHODS: A well-validated affective picture-viewing paradigm was used to study emotional modulation of pain in 33 healthy, pain-free SA survivors and a control group of 33 healthy, pain-free individuals with no reported history of SA (matched on age, sex, race, and number of non-SA traumas). Unpleasant (mutilation), neutral, and pleasant (erotica) pictures were presented while painful electrocutaneous stimulations were delivered at the ankle. Pain intensity ratings and nociceptive flexion reflex magnitudes (NFR; a physiologic measure of spinal nociception) were recorded in response to electric stimuli. Multilevel models were used to analyze the data with Group (SA vs. no-SA) and Content (mutilation, neutral, erotica) as IVs. RESULTS: Both groups demonstrated similar emotional modulation of pain [FGroupXContent(F(2,646.52)=0.44, p=.65], but a main effect of group [FGroup(1,65.42)=4.24, p=.043] indicated the SA group experienced more overall pain from electric stimuli (hyperalgesia). A significant Group X Content interaction for NFR (p=.035) indicated that emotional modulation of NFR was present for the no-SA group [FContentSimpleEffect(2,684.55)=12.43, p<.001], but not the SA group [FContentSimpleEffect(2,683.38)=1.71, p=.18]. CONCLUSIONS: These findings suggest SA survivors have difficulty emotionally engaging brain-to-spinal cord mechanisms to modulate spinal nociception. A disruption of descending inhibition plus hyperalgesia could contribute to comorbidity between sexual trauma and chronic pain.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1097/PSY.0000000000000567

  9 / 106032 MEDLINE  
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[PMID]: 28466274
[Au] Autor:Xiao J; Yang R; Biswas S; Zhu Y; Qin X; Zhang M; Zhai L; Luo Y; He X; Mao C; Deng W
[Ad] Address:Department of Neurology, Xiang Yang Central Hospital, Medical College of Hubei University of Arts and Science, Xiangyang, Hubei, China.
[Ti] Title:Neural Stem Cell-Based Regenerative Approaches for the Treatment of Multiple Sclerosis.
[So] Source:Mol Neurobiol;55(4):3152-3171, 2018 Apr.
[Is] ISSN:1559-1182
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Multiple sclerosis (MS) is a chronic, autoimmune, inflammatory, and demyelinating disorder of the central nervous system (CNS), which ultimately leads to axonal loss and permanent neurological disability. Current treatments for MS are largely comprised of medications that are either immunomodulatory or immunosuppressive and are aimed at reducing the frequency and intensity of relapses. Neural stem cells (NSCs) in the adult brain can differentiate into oligodendrocytes in a context-specific manner and are shown to be involved in the remyelination in these patients. NSCs may exert their beneficial effects not only through oligodendrocyte replacement but also by providing trophic support and immunomodulation, a phenomenon now known as "therapeutic plasticity." In this review, we first provided an update on the current knowledge regarding MS pathogenesis and the role of immune cells, microglia, and oligodendrocytes in MS disease progression. Next, we reviewed the current progress on research aimed toward stimulating endogenous NSC proliferation and differentiation to oligodendrocytes in vivo and in animal models of demyelination. In addition, we explored the neuroprotective and immunomodulatory effects of transplanted exogenous NSCs on T cell activation, microglial activation, and endogenous remyelination and their effects on the pathological process and prognosis in animal models of MS. Finally, we examined various protocols to generate genetically engineered NSCs as a potential therapy for MS. Overall, this review highlights the studies involving the immunomodulatory, neurotrophic, and regenerative effects of NSCs and novel methods aiming at stimulating the potential of NSCs for the treatment of MS.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1705
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1007/s12035-017-0566-7

  10 / 106032 MEDLINE  
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[PMID]: 29524326
[Au] Autor:Tanida M; Tao Z; Sun L; Song J; Yang W; Kuda Y; Kurata Y; Shibamoto T
[Ad] Address:Department of Physiology II, Kanazawa Medical University, Uchinada, Ishikawa, 920-0293, Japan.
[Ti] Title:Anaphylactic hypotension causes renal and adrenal sympathoexcitaion and induces c-fos in the hypothalamus and medulla oblongata: Anaphylaxis affects the brain and activates sympathetic nerves.
[So] Source:Exp Physiol;, 2018 Mar 10.
[Is] ISSN:1469-445X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:NEW FINDINGS: What is the central question of this study? Whether anaphylaxis affects sympathetic outflows to the brown adipose tissue (BAT) and adrenal grand is not known. Moreover, it is unknown whether anaphylaxis affects some brain areas in association with sympathetic regulation. What is the main finding and its importance? We showed that sympathoexcitatory responses to anaphylaxis regionally occurred in the kidney and adrenal grand, but not in the thermogenesis-related BAT. Further, anaphylactic hypotension also caused increase in c-fos immunoreactivity in the hypothalamic and medullary areas. Moreover, catecholaminergic neurons of the brain stem causes adrenal sympathoexcitation in a baroreceptor-independent manner. ABSTRACT: We previously reported that sympathetic nerve activity (SNA) to the kidney and the hind limb increases during anaphylactic hypotension in anesthetized rats. Based on this evidence, we examined effects of anaphylactic hypotension on SNA to the brown adipose tissue (BAT), and the adrenal gland and kidney in anesthetized rats. We demonstrated that adrenal and renal SNA, but not BAT-SNA, were stimulated. In addition, the effects of anaphylaxis on neural activities of the hypothalamic and medullary nuclei, which are candidates for relaying efferent SNA to the peripheral organs, were investigated via immunohistochemical staining of c-fos. Anaphylaxis increased c-fos expression in the neurons of the paraventricular nucleus (PVN) of the hypothalamus and in those of the nucleus tractus solitarius (NTS) and rostral ventrolateral medulla (RVLM) of the medulla oblongata; c-fos was expressed in gamma-aminobutyric acid (GABA)-ergic neurons of the NTS and in the catecholaminergic neurons of the RVLM. In addition, c-fos expression in the rostral NTS and mid NTS during anaphylaxis were reduced by sinoaortic baroreceptor denervation, however increased c-fos expression in the caudal NTS and RVLM or adrenal sympathoexcitation were not affected by sinoaortic baroreceptor denervation. These results indicated that anaphylactic hypotension activates the hypothalamic PVN, and the medullary NTS and RVLM, independently of the baroreflex pathway. Further, it stimulated efferent SNA to the adrenal grand and kidney to restore blood pressure. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1113/EP086809


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