| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Boonrat Chantong, Denise V Kratschmar, Adam Lister, Alex Odermat. Inhibition of metabotropic glutamate receptor 5 induces cellular stress through pertussis toxin-sensitive Gi-proteins in murine BV-2 microglia cells. Journal of neuroinflammation. vol 11. 2015-11-20. PMID:25407356. |
inhibition of metabotropic glutamate receptor 5 induces cellular stress through pertussis toxin-sensitive gi-proteins in murine bv-2 microglia cells. |
2015-11-20 |
2023-08-13 |
mouse |
| Boonrat Chantong, Denise V Kratschmar, Adam Lister, Alex Odermat. Inhibition of metabotropic glutamate receptor 5 induces cellular stress through pertussis toxin-sensitive Gi-proteins in murine BV-2 microglia cells. Journal of neuroinflammation. vol 11. 2015-11-20. PMID:25407356. |
activation of metabotropic glutamate receptor 5 (mglur5) by (rs)-2-chloro-5-hydroxyphenylglycine (chpg) was shown to suppress microglia activation and decrease the release of associated pro-inflammatory mediators. |
2015-11-20 |
2023-08-13 |
mouse |
| Tetsuya Mizun. [Neuronal dysfunction in multiple sclerosis]. Rinsho shinkeigaku = Clinical neurology. vol 54. issue 12. 2015-10-19. PMID:25519963. |
microglia produce various inflammatory cytokines such as ifn-γ and il-β, reactive oxygen species, and glutamate. |
2015-10-19 |
2023-08-13 |
Not clear |
| B Amin, V Hajhashemi, H Hosseinzade. Minocycline potentiates the anti-hyperalgesic effect of ceftriaxone in CCI-induced neuropathic pain in rats. Research in pharmaceutical sciences. vol 10. issue 1. 2015-10-02. PMID:26430455. |
the purpose of the present study was to evaluate anti-hyperalgesic effect of repeated administration of ceftriaxone, which selectively activates and increases the expression of glutamate transporter, as well as minocycline, a selective inhibitor of microglia activation, either alone or together in wistar rats subjected to the chronic constriction injury (cci) of sciatic nerve. |
2015-10-02 |
2023-08-13 |
rat |
| Xiao Z Shen, You Li, Liang Li, Kandarp H Shah, Kenneth E Bernstein, Patrick Lyden, Peng Sh. Microglia participate in neurogenic regulation of hypertension. Hypertension (Dallas, Tex. : 1979). vol 66. issue 2. 2015-09-30. PMID:26056339. |
targeted depletion of microglia significantly attenuated neuroinflammation, glutamate receptor expression in the paraventricular nucleus, plasma vasopressin level, kidney norepinephrine concentration, and blood pressure. |
2015-09-30 |
2023-08-13 |
mouse |
| Renato Socodato, Camila C Portugal, Ivan Domith, Nádia A Oliveira, Vivian S M Coreixas, Erick C Loiola, Tânia Martins, Ana Raquel Santiago, Roberto Paes-de-Carvalho, António F Ambrósio, João B Relva. c-Src function is necessary and sufficient for triggering microglial cell activation. Glia. vol 63. issue 3. 2015-09-21. PMID:25421817. |
in this study, using both in vivo and in vitro inflammation models coupled to fret-based time-lapse microscopy, lentiviruses-mediated shrna delivery and genetic gain-of-function experiments, we demonstrate that among sfks c-src function is necessary and sufficient for triggering microglia proinflammatory signature, glutamate release, microglia-induced neuronal loss, and phagocytosis. |
2015-09-21 |
2023-08-13 |
Not clear |
| Kazuyuki Nakajima, Tomoyuki Kanamatsu, Yosuke Takezawa, Shinichi Kohsak. Up-regulation of glutamine synthesis in microglia activated with endotoxin. Neuroscience letters. vol 591. 2015-09-15. PMID:25681623. |
we previously verified that newborn rat brain-derived microglia have the ability to uptake (14)c-glutamate (glu) through glutamate transporter-1. |
2015-09-15 |
2023-08-13 |
rat |
| Fang Liu, Yunlong Huang, Fang Zhang, Qiang Chen, Beiqing Wu, Wei Rui, Jialin C Zheng, Wenjun Din. Macrophages treated with particulate matter PM2.5 induce selective neurotoxicity through glutaminase-mediated glutamate generation. Journal of neurochemistry. vol 134. issue 2. 2015-09-14. PMID:25913161. |
these macrophages and microglia significantly increased extracellular levels of glutamate following pm2.5 exposure, which were negatively correlated with neuronal viability. |
2015-09-14 |
2023-08-13 |
Not clear |
| Kirsten S Evonuk, Brandi J Baker, Ryan E Doyle, Carson E Moseley, Christine M Sestero, Bryce P Johnston, Patrizia De Sarno, Andrew Tang, Igor Gembitsky, Sandra J Hewett, Casey T Weaver, Chander Raman, Tara M DeSilv. Inhibition of System Xc(-) Transporter Attenuates Autoimmune Inflammatory Demyelination. Journal of immunology (Baltimore, Md. : 1950). vol 195. issue 2. 2015-09-09. PMID:26071560. |
primary coculture studies demonstrate that myelin-specific cd4(+) th1 cells provoke microglia to release glutamate via the system xc(-) transporter, causing excitotoxic death to mature myelin-producing oligodendrocytes. |
2015-09-09 |
2023-08-13 |
mouse |
| Akio Suzumur. [Microglia in neurodegenerative disorders and neuroinflammation]. Rinsho shinkeigaku = Clinical neurology. vol 54. issue 12. 2015-08-17. PMID:25672725. |
we previously showed that glutamate is the most neurotoxic factor released by activated microglia, and suppressing glutamate release from microglia can inhibit disease progression in various animal models of neurodegenerative disorders. |
2015-08-17 |
2023-08-13 |
Not clear |
| Fumito Endo, Koji Yamanak. [Neuroinflammation in amyotrophic lateral sclerosis]. Rinsho shinkeigaku = Clinical neurology. vol 54. issue 12. 2015-08-17. PMID:25672727. |
since microglia produce proinflammatory cytokines and other neurotoxic or protective molecules and astrocytes reduce their glutamate uptake, these functional changes in glial cells are considered to play important roles in neurodegeneration. |
2015-08-17 |
2023-08-13 |
Not clear |
| Daisuke Umebayashi, Atsushi Natsume, Hideyuki Takeuchi, Masahito Hara, Yusuke Nishimura, Ryuichi Fukuyama, Naoyuki Sumiyoshi, Toshihiko Wakabayash. Blockade of gap junction hemichannel protects secondary spinal cord injury from activated microglia-mediated glutamate exitoneurotoxicity. Journal of neurotrauma. vol 31. issue 24. 2015-08-03. PMID:24588281. |
we previously demonstrated that activated microglia release excessive glutamate through gap junction hemichannels and identified a novel gap junction hemichannel blocker, ini-0602, that was proven to penetrate the blood-brain barrier and be an effective treatment in mouse models of amyotrophic lateral sclerosis and alzheimer disease. |
2015-08-03 |
2023-08-12 |
mouse |
| Daisuke Umebayashi, Atsushi Natsume, Hideyuki Takeuchi, Masahito Hara, Yusuke Nishimura, Ryuichi Fukuyama, Naoyuki Sumiyoshi, Toshihiko Wakabayash. Blockade of gap junction hemichannel protects secondary spinal cord injury from activated microglia-mediated glutamate exitoneurotoxicity. Journal of neurotrauma. vol 31. issue 24. 2015-08-03. PMID:24588281. |
activated microglia release glutamate, the major neurotoxic factor released into the extracellular space after neural injury, which causes neuronal death at high concentration. |
2015-08-03 |
2023-08-12 |
mouse |
| Lucía Calatrava-Ferreras, Rafael Gonzalo-Gobernado, Diana Reimers, Antonio S Herranz, Adriano Jiménez-Escrig, Juan José Díaz-Gil, María José Casarejos, María Teresa Montero-Vega, Eulalia Bazá. Neuroprotective role of liver growth factor "LGF" in an experimental model of cerebellar ataxia. International journal of molecular sciences. vol 15. issue 10. 2015-06-19. PMID:25338046. |
lgf also reduced extracellular glutamate and gaba concentrations and microglia activation in the cerebellum. |
2015-06-19 |
2023-08-13 |
rat |
| Felicita Pedata, Anna Maria Pugliese, Elisabetta Coppi, Ilaria Dettori, Giovanna Maraula, Lucrezia Cellai, Alessia Melan. Adenosine A2A receptors modulate acute injury and neuroinflammation in brain ischemia. Mediators of inflammation. vol 2014. 2015-05-15. PMID:25165414. |
after ischemia the early massive increase of extracellular glutamate is followed by activation of resident immune cells, that is, microglia, and production or activation of inflammation mediators. |
2015-05-15 |
2023-08-13 |
Not clear |
| Robert Dantzer, Adam K Walke. Is there a role for glutamate-mediated excitotoxicity in inflammation-induced depression? Journal of neural transmission (Vienna, Austria : 1996). vol 121. issue 8. 2015-05-12. PMID:24633997. |
quinolinic acid can synergize with glutamate released by activated microglia. |
2015-05-12 |
2023-08-12 |
Not clear |
| Robert Dantzer, Adam K Walke. Is there a role for glutamate-mediated excitotoxicity in inflammation-induced depression? Journal of neural transmission (Vienna, Austria : 1996). vol 121. issue 8. 2015-05-12. PMID:24633997. |
this chain of events opens the possibility to treat inflammation-induced depression using therapies that target the transport of kynurenine through the blood-brain barrier, the production of quinolinic acid and glutamate by activated microglia, or the efflux of glutamate from the brain to the blood. |
2015-05-12 |
2023-08-12 |
Not clear |
| Ivana R Stojanovic, Milos Kostic, Srdjan Ljubisavljevi. The role of glutamate and its receptors in multiple sclerosis. Journal of neural transmission (Vienna, Austria : 1996). vol 121. issue 8. 2015-05-12. PMID:24633998. |
glutamate is an excitatory neurotransmitter of the central nervous system, which has a central role in a complex communication network established between neurons, astrocytes, oligodendrocytes, and microglia. |
2015-05-12 |
2023-08-12 |
Not clear |
| Lee-Way Jin, Makoto Horiuchi, Heike Wulff, Xiao-Bo Liu, Gino A Cortopassi, Jeffrey D Erickson, Izumi Maezaw. Dysregulation of glutamine transporter SNAT1 in Rett syndrome microglia: a mechanism for mitochondrial dysfunction and neurotoxicity. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 35. issue 6. 2015-04-13. PMID:25673846. |
because glutamine is mainly metabolized in the mitochondria, where it is used as an energy substrate and a precursor for glutamate production, we hypothesize that snat1 overexpression in mecp2-deficient microglia would impair the glutamine homeostasis, resulting in mitochondrial dysfunction as well as microglial neurotoxicity because of glutamate overproduction. |
2015-04-13 |
2023-08-13 |
mouse |
| Lee-Way Jin, Makoto Horiuchi, Heike Wulff, Xiao-Bo Liu, Gino A Cortopassi, Jeffrey D Erickson, Izumi Maezaw. Dysregulation of glutamine transporter SNAT1 in Rett syndrome microglia: a mechanism for mitochondrial dysfunction and neurotoxicity. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 35. issue 6. 2015-04-13. PMID:25673846. |
supporting this hypothesis, we found that mecp2 downregulation or snat1 overexpression in microglia resulted in (1) glutamine-dependent decrease in microglial viability, which was corroborated by reduced microglia counts in the brains of mecp2 knock-out mice; (2) proliferation of mitochondria and enhanced mitochondrial production of reactive oxygen species; (3) increased oxygen consumption but decreased atp production (an energy-wasting state); and (4) overproduction of glutamate that caused nmda receptor-dependent neurotoxicity. |
2015-04-13 |
2023-08-13 |
mouse |