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[PMID]: 29506554
[Au] Autor:Vizuete AFK; Hansen F; Negri E; Leite MC; de Oliveira DL; Gonçalves CA
[Ad] Address:Department of Biochemistry, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600-Anexo, Porto Alegre, RS, 90035-003, Brazil. adrianavizuete@gmail.com.
[Ti] Title:Effects of dexamethasone on the Li-pilocarpine model of epilepsy: protection against hippocampal inflammation and astrogliosis.
[So] Source:J Neuroinflammation;15(1):68, 2018 Mar 05.
[Is] ISSN:1742-2094
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Temporal lobe epilepsy (TLE) is the most common form of partial epilepsy and is accompanied, in one third of cases, by resistance to antiepileptic drugs (AED). Most AED target neuronal activity modulated by ionic channels, and the steroid sensitivity of these channels has supported the use of corticosteroids as adjunctives to AED. Assuming the importance of astrocytes in neuronal activity, we investigated inflammatory and astroglial markers in the hippocampus, a key structure affected in TLE and in the Li-pilocarpine model of epilepsy. METHODS: Initially, hippocampal slices were obtained from sham rats and rats subjected to the Li-pilocarpine model of epilepsy, at 1, 14, and 56 days after status epilepticus (SE), which correspond to the acute, silent, and chronic phases. Dexamethasone was added to the incubation medium to evaluate the secretion of S100B, an astrocyte-derived protein widely used as a marker of brain injury. In the second set of experiments, we evaluated the in vivo effect of dexamethasone, administrated at 2 days after SE, on hippocampal inflammatory (COX-1/2, PGE2, and cytokines) and astroglial parameters: GFAP, S100B, glutamine synthetase (GS) and water (AQP-4), and K (Kir 4.1) channels. RESULTS: Basal S100B secretion and S100B secretion in high-K medium did not differ at 1, 14, and 56 days for the hippocampal slices from epileptic rats, in contrast to sham animal slices, where high-K medium decreased S100B secretion. Dexamethasone addition to the incubation medium per se induced a decrease in S100B secretion in sham and epileptic rats (1 and 56 days after SE induction). Following in vivo dexamethasone administration, inflammatory improvements were observed, astrogliosis was prevented (based on GFAP and S100B content), and astroglial dysfunction was partially abrogated (based on Kir 4.1 protein and GSH content). The GS decrease was not prevented by dexamethasone, and AQP-4 was not altered in this epileptic model. CONCLUSIONS: Changes in astroglial parameters emphasize the importance of these cells for understanding alterations and mechanisms of epileptic disorders in this model. In vivo dexamethasone administration prevented most of the parameters analyzed, reinforcing the importance of anti-inflammatory steroid therapy in the Li-pilocarpine model and possibly in other epileptic conditions in which neuroinflammation is present.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s12974-018-1109-5

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[PMID]: 29474875
[Au] Autor:Li L; Yang R; Feng M; Guo Y; Wang Y; Guo J; Lu X
[Ad] Address:Department of Geriatrics, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210011, Jiangsu, China; Department of Geriatrics, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, 221002, China.
[Ti] Title:Rig-I is involved in inflammation through the IPS-1/TRAF pathway in astrocytes under chemical hypoxia.
[So] Source:Neurosci Lett;672:46-52, 2018 Feb 21.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:The retinoic acid-inducible gene I (RIG-I) is a crucial cytoplasmic pathogen recognition receptor involved in neuroinflammation in degenerative diseases. In the present study, in vitro human astrocytes were subjected to a chemical hypoxia model using cobalt chloride pretreatment. Chemical hypoxia induces the up-regulation of RIG-I in astrocytes and results in the expression of inflammatory cytokines IL-1ß, IL-6, and TNF-α in an NF-κB dependent manner. Elevated RIG-I modulates the interaction of interferon-ß promoter stimulator-1 (IPS-1) and TNF receptor-associated factor 6 (TRAF6) following chemical hypoxia. Inhibition of IPS-1 or TRAF6 suppresses RIG-I-induced NF-κB activation and inflammatory cytokines in response to chemical hypoxia. These data suggest that chemical hypoxia leads to RIG-I activation and the expression of inflammatory cytokines through the NF-κB pathway. Blocking IPS-1/TRAF6 pathway relieves RIG-I-induced neuroinflammation in astrocytes subjected to hypoxia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 48385 MEDLINE  
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[PMID]: 29462638
[Au] Autor:Manzhulo I; Tyrtyshnaia A; Kipryushina Y; Dyuizen I; Ermolenko E; Manzhulo O
[Ad] Address:National Scientific Center of Marine Biology, Far Eastern Branch, Russian Academy of Sciences, Vladivostok, 690041, Russia; School of Biomedicine, Far Eastern Federal University, Vladivostok, 690950, Russia. Electronic address: i-manzhulo@bk.ru.
[Ti] Title:Docosahexaenoic acid improves motor function in the model of spinal cord injury.
[So] Source:Neurosci Lett;672:6-14, 2018 Feb 17.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:The present study demonstrates that docosahexaenoic acid (DHA, 22:6n-3) injected subcutaneously leads to recovery of locomotor functions observed within 5 weeks after traumatic spinal cord injury. This activity is confirmed by improving of BBB locomotor rating scale indicators. We assume that this activity is related to (1) enhancement of remyelination process, (2) proliferative activity, (3) antioxidant activity, (4) increase in GFAP staining and (5) enhancement of vimentin expression. In general, the results of the study show that DHA has a complex effect on post-traumatic central nervous system recovery, indicating its high therapeutic potential.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 48385 MEDLINE  
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[PMID]: 29424334
[Au] Autor:Kearney H; Cryan J; Beausang A; Looby S; Brett FM
[Ti] Title:Reactive gliosis mimicking tumor recurrence - a case series documenting MRI abnormalities and neuropathological correlates.
[So] Source:Clin Neuropathol;, 2018 02 09.
[Is] ISSN:0722-5091
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:The aim of this study is to identify, in our center, all cases of foreign-body reactions to hemostatic agents or other prostheses resulting in a radiological suspicion of tumor recurrence. We interrogated our internal database to identify all such cases and systematically evaluated the MRI brain scans of patients: (i) at the time of initial tumor diagnosis, (ii) postoperatively, (iii) and at the time of suspected tumor recurrence. In addition, we reviewed each patient's operative notes and reviewed the histology of all cases following a second surgical intervention. In total, we identified 8 patients, 7 of whom had a WHO grade II glioma at initial surgery. We did not identify any distinguishing radiological abnormalities from the initial diagnostic brain scan to the suspected recurrence, and histologically all cases were characterized by extensive gliosis; with both macrophages and reactive astrocytes present throughout. The cause of gliosis was identified as being relating to hemostatic agents in 4 cases; in the other 4 cases, the foreign-body reaction was presumed to be caused be materials used in a craniotomy or cranioplasty. This study highlights the difficulty in radiologically diagnosing a foreign-body reaction and also identifies that such a gliotic reaction may occur as a consequence of exogenous materials used in a craniotomy or cranioplasty.
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[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.5414/NP301084

  5 / 48385 MEDLINE  
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[PMID]: 29203121
[Au] Autor:Korol DL; Wang W
[Ad] Address:Department of Biology, Syracuse University, Syracuse, NY 13244, United States. Electronic address: dlkorol@syr.edu.
[Ti] Title:Using a memory systems lens to view the effects of estrogens on cognition: Implications for human health.
[So] Source:Physiol Behav;187:67-78, 2018 Apr 01.
[Is] ISSN:1873-507X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Understanding the organizing and activating effects of gonadal steroids on adult physiology can guide insight into sex differences in and hormonal influences on health and disease, ranging from diabetes and other metabolic disorders, emotion and stress regulation, substance abuse, pain perception, immune function and inflammation, to cognitive function and dysfunction accompanying neurological disorders. Because the brain is highly sensitive to many forms of estrogens, it is not surprising that many adult behaviors, including cognitive function, are modulated by estrogens. Estrogens are known for their facilitating effects on learning and memory, but it is becoming increasingly clear that they also can impair learning and memory of some classes of tasks and may do so through direct actions on specific neural systems. This review takes a multiple memory systems approach to understanding how estrogens can at the same time enhance hippocampus-sensitive place learning and impair striatum-sensitive response learning by exploring the role estrogen receptor signaling may play in the opposing cognitive effects of estrogens. Accumulating evidence suggests that neither receptor subtype nor the timing of treatment, i.e. rapid vs slow, explain the bidirectional effects of estrogens on different types of learning. New findings pointing to neural metabolism and the provision of energy substrates by astrocytes as a candidate mechanism for cognitive enhancement and impairment are discussed.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  6 / 48385 MEDLINE  
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[PMID]: 29524214
[Au] Autor:Shiotani H; Miyata M; Itoh Y; Wang S; Kaito A; Mizoguchi A; Yamasaki M; Watanabe M; Mandai K; Mochizuki H; Takai Y
[Ad] Address:Division of Pathogenetic Signaling, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0047, Japan.
[Ti] Title:Localization of nectin-2α at the boundary between the adjacent somata of the clustered cholinergic neurons and its regulatory role in the subcellular localization of the voltage-gated A-type K channel Kv4.2 in the medial habenula.
[So] Source:J Comp Neurol;, 2018 Mar 09.
[Is] ISSN:1096-9861
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The medial habenula (MHb), implicated in stress, depression, memory, and nicotine withdrawal syndromes, receives septal inputs and sends efferents to the interpeduncular nucleus. We previously showed that the immunoglobulin-like cell adhesion molecules nectin-2α and nectin-2δ are expressed in astrocytes in the brain, but their expression in neurons remains unknown. We showed here by immunofluorescence microscopy that nectin-2α, but not nectin-2δ, was prominently expressed in the cholinergic neurons in the developing and adult MHbs and localized at the boundary between the adjacent somata of the clustered cholinergic neurons where the voltage-gated A-type K channel Kv4.2 was localized. Analysis by immunoelectron microscopy on this boundary revealed that Kv4.2 was localized at the membrane specializations with plasma membrane darkening in an asymmetrical manner, whereas nectin-2α was localized on the apposed plasma membranes mostly at the outside of these membrane specializations, but occasionally localized at their edges and insides. Nectin-2α at this boundary was not colocalized with the nectin-2α-binding protein afadin, other cell adhesion molecules, or their interacting peripheral membrane proteins, suggesting that nectin-2α forms a cell adhesion apparatus different from the Kv4.2-associated membrane specializations. Genetic ablation of nectin-2 delayed the localization of Kv4.2 at the boundary between the adjacent somata of the clustered cholinergic neurons in the developing MHb. These results revealed the unique localization of nectin-2α and its regulatory role in the localization of Kv4.2 at the membrane specializations in the MHb. 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:10.1002/cne.24425

  7 / 48385 MEDLINE  
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[PMID]: 29523880
[Au] Autor:Rincon MY; de Vin F; Duqué SI; Fripont S; Castaldo SA; Bouhuijzen-Wenger J; Holt MG
[Ad] Address:VIB-KU Leuven Center for Brain & Disease Research, Leuven, Belgium.
[Ti] Title:Widespread transduction of astrocytes and neurons in the mouse central nervous system after systemic delivery of a self-complementary AAV-PHP.B vector.
[So] Source:Gene Ther;, 2018 Mar 09.
[Is] ISSN:1476-5462
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Until recently, adeno-associated virus 9 (AAV9) was considered the AAV serotype most effective in crossing the blood-brain barrier (BBB) and transducing cells of the central nervous system (CNS), following systemic injection. However, a newly engineered capsid, AAV-PHP.B, is reported to cross the BBB at even higher efficiency. We investigated how much we could boost CNS transgene expression by using AAV-PHP.B carrying a self-complementary (sc) genome. To allow comparison, 6 weeks old C57BL/6 mice received intravenous injections of scAAV2/9-GFP or scAAV2/PHP.B-GFP at equivalent doses. Three weeks postinjection, transgene expression was assessed in brain and spinal cord. We consistently observed more widespread CNS transduction and higher levels of transgene expression when using the scAAV2/PHP.B-GFP vector. In particular, we observed an unprecedented level of astrocyte transduction in the cortex, when using a ubiquitous CBA promoter. In comparison, neuronal transduction was much lower than previously reported. However, strong neuronal expression (including spinal motor neurons) was observed when the human synapsin promoter was used. These findings constitute the first reported use of an AAV-PHP.B capsid, encapsulating a scAAV genome, for gene transfer in adult mice. Our results underscore the potential of this AAV construct as a platform for safer and more efficacious gene therapy vectors for the CNS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1038/s41434-018-0005-z

  8 / 48385 MEDLINE  
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[PMID]: 29523207
[Au] Autor:Mutemberezi V; Buisseret B; Masquelier J; Guillemot-Legris O; Alhouayek M; Muccioli GG
[Ad] Address:Bioanalysis and Pharmacology of Bioactive Lipids Research Group, Louvain Drug Research Institute (LDRI), Université catholique de Louvain (UCL), Av. E. Mounier, 72 (B1.72.01), 1200, Bruxelles, Belgium.
[Ti] Title:Oxysterol levels and metabolism in the course of neuroinflammation: insights from in vitro and in vivo models.
[So] Source:J Neuroinflammation;15(1):74, 2018 Mar 09.
[Is] ISSN:1742-2094
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Oxysterols are cholesterol derivatives that have been suggested to play a role in inflammatory diseases such as obesity, atherosclerosis, or neuroinflammatory diseases. However, the effect of neuroinflammation on oxysterol levels has only been partially studied so far. METHODS: We used an HPLC-MS method to quantify over ten oxysterols both in in vitro and in vivo models of neuroinflammation. In the same models, we used RT-qPCR to analyze the expression of the enzymes responsible for oxysterol metabolism. Using the BV2 microglial cell line, we explored the effect of lipopolysaccharide (LPS)-induced (M1-type) and IL-4-induced (M2-type) cell activation on oxysterol levels. We also used LPS-activated co-cultures of mouse primary microglia and astrocytes. In vivo, we induced a neuroinflammation by administering LPS to mice. Finally, we used a mouse model of multiple sclerosis, namely the experimental autoimmune encephalomyelitis (EAE) model, that is characterized by demyelination and neuroinflammation. RESULTS: In vitro, we found that LPS activation induces profound alterations in oxysterol levels. Interestingly, we could discriminate between control and LPS-activated cells based on the changes in oxysterol levels both in BV2 cells and in the primary co-culture of glial cells. In vivo, the changes in oxysterol levels were less marked than in vitro. However, we found in both models increased levels of the GPR183 agonist 7α,25-dihydroxycholesterol. Furthermore, we studied in vitro the effect of 14 oxysterols on the mRNA expression of inflammatory markers in LPS-activated co-culture of microglia and astrocytes. We found that several oxysterols decreased the LPS-induced expression of pro-inflammatory markers. CONCLUSIONS: These data demonstrate that inflammation profoundly affects oxysterol levels and that oxysterols can modulate glial cell activation. This further supports the interest of a large screening of oxysterol levels when studying the interplay between neuroinflammation and bioactive lipids.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1186/s12974-018-1114-8

  9 / 48385 MEDLINE  
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[PMID]: 29501892
[Au] Autor:Wellman SM; Kozai TDY
[Ad] Address:Department of Bioengineering, University of Pittsburgh, United States; Center for the Basis of Neural Cognition, United States.
[Ti] Title:In vivo spatiotemporal dynamics of NG2 glia activity caused by neural electrode implantation.
[So] Source:Biomaterials;164:121-133, 2018 May.
[Is] ISSN:1878-5905
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Neural interface technology provides direct sampling and analysis of electrical and chemical events in the brain in order to better understand neuronal function and treat neurodegenerative disease. However, intracortical electrodes experience inflammatory reactions that reduce long-term stability and functionality and are understood to be facilitated by activated microglia and astrocytes. Emerging studies have identified another cell type that participates in the formation of a high-impedance glial scar following brain injury; the oligodendrocyte precursor cell (OPC). These cells maintain functional synapses with neurons and are a crucial source of neurotrophic support. Following injury, OPCs migrate toward areas of tissue injury over the course of days, similar to activated microglia. The delayed time course implicates these OPCs as key components in the formation of the outer layers of the glial scar around the implant. In vivo two-photon laser scanning microscopy (TPLSM) was employed to observe fluorescently-labeled OPC and microglia reactivity up to 72 h following probe insertion. OPCs initiated extension of cellular processes (2.5 ±â€¯0.4 µm h ) and cell body migration (1.6 ±â€¯0.3 µm h ) toward the probe beginning 12 h after insertion. By 72 h, OPCs became activated at a radius of about 190.3 µm away from the probe surface. This study characterized the early spatiotemporal dynamics of OPCs involved in the inflammatory response induced by microelectrode insertion. OPCs are key mediators of tissue health and are understood to have multiple fate potentials. Detailed spatiotemporal characterization of glial behavior under pathological conditions may allow identification of alternative intervention targets for mitigating the formation of a glial scar and subsequent neurodegeneration that debilitates chronic neural interfaces.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review

  10 / 48385 MEDLINE  
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[PMID]: 29477834
[Au] Autor:Wu X; Liu S; Hu Z; Zhu G; Zheng G; Wang G
[Ad] Address:Department of Anesthesiology, Henan Provincial People's Hospital, Zhengzhou, Henan, 450003, PR China.
[Ti] Title:Enriched housing promotes post-stroke neurogenesis through calpain 1-STAT3/HIF-1α/VEGF signaling.
[So] Source:Brain Res Bull;139:133-143, 2018 Feb 26.
[Is] ISSN:1873-2747
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Enriched environment (EE) has been shown to promote neurogenesis and functional recovery after ischemic stroke. However, the underlying molecular mechanisms are not fully understood. In this study, C57BL/6 mice underwent middle cerebral artery occlusion (60 min) followed by reperfusion, after which mice were housed in either standard environment (SE) or EE and allowed to survive for 3, 4, 6 or 10 weeks. Ipsilateral subventricular zone (SVZ) or striatum cells were dissociated from ischemic hemispheric brains of enriched mice at 14 days post-ischemia (dpi) and cultured in vitro. Our data showed that post-ischemic EE inhibited calpain 1 activity, and increased the expression of phosphorylated signal transducer and activator of transcription 3 (p-STAT3) in the ischemic hemisphere of enriched mice at 21 dpi. Calpain 1-specific inhibitor PD151746 further increased p-STAT3 expression and augmented the promoting effects of EE on post-stroke SVZ neural precursor cells (NPCs) proliferation and functional recovery. EE also increased the expression of hypoxia-inducible factor 1-alpha (HIF-1α) and vascular endothelial growth factor (VEGF) in the ischemic hemisphere at 21 dpi. Inhibition of the JAK/STAT3 pathway with AG490 decreased the expression of HIF-1α and VEGF. Furthermore, inhibition of HIF-1α with 2-methoxyestradiol robustly abolished EE-induced elevation of VEGF l expression. Furthermore, VEGF-A promoted the production and secretion of high mobility group box-1 protein (HMGB1) from reactive astrocytes in vitro. Culture supernatant from reactive astrocytes treated with VEGF-A promoted the proliferation and differentiation of NPCs. Glycyrrhizin reversed the promoting effects of EE on post-stroke neurorepair and functional recovery in vivo. Taken together, our data indicate that EE promotes post-stroke functional recovery through the inhibition of calpain 1 activity, and subsequent STAT3-HIF-1α-VEGF-mediated neurogenesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher


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