Delayed mGluR5 activation limits neuroinflammation and neurodegeneration after traumatic brain injury
Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss may continue for months or years after traumatic brain injury in association with chronic microglial activation. Recently we found that metabotropic glutamate rec...
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| Published in | Journal of neuroinflammation Vol. 9; no. 1; p. 43 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
BioMed Central Ltd
28.02.2012
BioMed Central BMC |
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| Online Access | Get full text |
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| Abstract | Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss may continue for months or years after traumatic brain injury in association with chronic microglial activation. Recently we found that metabotropic glutamate receptor 5 (mGluR5) activation by (RS)-2-chloro-5-hydroxyphenylglycine (CHPG) decreases microglial activation and release of associated pro-inflammatory factors in vitro, which is mediated in part through inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Here we examined whether delayed CHPG administration reduces chronic neuroinflammation and associated neurodegeneration after experimental traumatic brain injury in mice.
One month after controlled cortical impact traumatic brain injury, C57Bl/6 mice were randomly assigned to treatment with single dose intracerebroventricular CHPG, vehicle or CHPG plus a selective mGluR5 antagonist, 3-((2-Methyl-4-thiazolyl)ethynyl)pyridine. Lesion volume, white matter tract integrity and neurological recovery were assessed over the following three months.
Traumatic brain injury resulted in mGluR5 expression in reactive microglia of the cortex and hippocampus at one month post-injury. Delayed CHPG treatment reduced expression of reactive microglia expressing NADPH oxidase subunits; decreased hippocampal neuronal loss; limited lesion progression, as measured by repeated T2-weighted magnetic resonance imaging (at one, two and three months) and white matter loss, as measured by high field ex vivo diffusion tensor imaging at four months; and significantly improved motor and cognitive recovery in comparison to the other treatment groups.
Markedly delayed, single dose treatment with CHPG significantly improves functional recovery and limits lesion progression after experimental traumatic brain injury, likely in part through actions at mGluR5 receptors that modulate neuroinflammation. |
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| AbstractList | Abstract Background Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss may continue for months or years after traumatic brain injury in association with chronic microglial activation. Recently we found that metabotropic glutamate receptor 5 (mGluR5) activation by (RS)-2-chloro-5-hydroxyphenylglycine (CHPG) decreases microglial activation and release of associated pro-inflammatory factors in vitro, which is mediated in part through inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Here we examined whether delayed CHPG administration reduces chronic neuroinflammation and associated neurodegeneration after experimental traumatic brain injury in mice. Methods One month after controlled cortical impact traumatic brain injury, C57Bl/6 mice were randomly assigned to treatment with single dose intracerebroventricular CHPG, vehicle or CHPG plus a selective mGluR5 antagonist, 3-((2-Methyl-4-thiazolyl)ethynyl)pyridine. Lesion volume, white matter tract integrity and neurological recovery were assessed over the following three months. Results Traumatic brain injury resulted in mGluR5 expression in reactive microglia of the cortex and hippocampus at one month post-injury. Delayed CHPG treatment reduced expression of reactive microglia expressing NADPH oxidase subunits; decreased hippocampal neuronal loss; limited lesion progression, as measured by repeated T2-weighted magnetic resonance imaging (at one, two and three months) and white matter loss, as measured by high field ex vivo diffusion tensor imaging at four months; and significantly improved motor and cognitive recovery in comparison to the other treatment groups. Conclusion Markedly delayed, single dose treatment with CHPG significantly improves functional recovery and limits lesion progression after experimental traumatic brain injury, likely in part through actions at mGluR5 receptors that modulate neuroinflammation. Background Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss may continue for months or years after traumatic brain injury in association with chronic microglial activation. Recently we found that metabotropic glutamate receptor 5 (mGluR5) activation by (RS)-2-chloro-5-hydroxyphenylglycine (CHPG) decreases microglial activation and release of associated pro-inflammatory factors in vitro, which is mediated in part through inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Here we examined whether delayed CHPG administration reduces chronic neuroinflammation and associated neurodegeneration after experimental traumatic brain injury in mice. Methods One month after controlled cortical impact traumatic brain injury, C57Bl/6 mice were randomly assigned to treatment with single dose intracerebroventricular CHPG, vehicle or CHPG plus a selective mGluR5 antagonist, 3-((2-Methyl-4-thiazolyl)ethynyl)pyridine. Lesion volume, white matter tract integrity and neurological recovery were assessed over the following three months. Results Traumatic brain injury resulted in mGluR5 expression in reactive microglia of the cortex and hippocampus at one month post-injury. Delayed CHPG treatment reduced expression of reactive microglia expressing NADPH oxidase subunits; decreased hippocampal neuronal loss; limited lesion progression, as measured by repeated T2-weighted magnetic resonance imaging (at one, two and three months) and white matter loss, as measured by high field ex vivo diffusion tensor imaging at four months; and significantly improved motor and cognitive recovery in comparison to the other treatment groups. Conclusion Markedly delayed, single dose treatment with CHPG significantly improves functional recovery and limits lesion progression after experimental traumatic brain injury, likely in part through actions at mGluR5 receptors that modulate neuroinflammation. Doc number: 43 Abstract Background: Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss may continue for months or years after traumatic brain injury in association with chronic microglial activation. Recently we found that metabotropic glutamate receptor 5 (mGluR5) activation by (RS )-2-chloro-5-hydroxyphenylglycine (CHPG) decreases microglial activation and release of associated pro-inflammatory factors in vitro , which is mediated in part through inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Here we examined whether delayed CHPG administration reduces chronic neuroinflammation and associated neurodegeneration after experimental traumatic brain injury in mice. Methods: One month after controlled cortical impact traumatic brain injury, C57Bl/6 mice were randomly assigned to treatment with single dose intracerebroventricular CHPG, vehicle or CHPG plus a selective mGluR5 antagonist, 3-((2-Methyl-4-thiazolyl)ethynyl)pyridine. Lesion volume, white matter tract integrity and neurological recovery were assessed over the following three months. Results: Traumatic brain injury resulted in mGluR5 expression in reactive microglia of the cortex and hippocampus at one month post-injury. Delayed CHPG treatment reduced expression of reactive microglia expressing NADPH oxidase subunits; decreased hippocampal neuronal loss; limited lesion progression, as measured by repeated T2-weighted magnetic resonance imaging (at one, two and three months) and white matter loss, as measured by high field ex vivo diffusion tensor imaging at four months; and significantly improved motor and cognitive recovery in comparison to the other treatment groups. Conclusion: Markedly delayed, single dose treatment with CHPG significantly improves functional recovery and limits lesion progression after experimental traumatic brain injury, likely in part through actions at mGluR5 receptors that modulate neuroinflammation. Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss may continue for months or years after traumatic brain injury in association with chronic microglial activation. Recently we found that metabotropic glutamate receptor 5 (mGluR5) activation by (RS)-2-chloro-5-hydroxyphenylglycine (CHPG) decreases microglial activation and release of associated pro-inflammatory factors in vitro, which is mediated in part through inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Here we examined whether delayed CHPG administration reduces chronic neuroinflammation and associated neurodegeneration after experimental traumatic brain injury in mice. One month after controlled cortical impact traumatic brain injury, C57Bl/6 mice were randomly assigned to treatment with single dose intracerebroventricular CHPG, vehicle or CHPG plus a selective mGluR5 antagonist, 3-((2-Methyl-4-thiazolyl)ethynyl)pyridine. Lesion volume, white matter tract integrity and neurological recovery were assessed over the following three months. Traumatic brain injury resulted in mGluR5 expression in reactive microglia of the cortex and hippocampus at one month post-injury. Delayed CHPG treatment reduced expression of reactive microglia expressing NADPH oxidase subunits; decreased hippocampal neuronal loss; limited lesion progression, as measured by repeated T2-weighted magnetic resonance imaging (at one, two and three months) and white matter loss, as measured by high field ex vivo diffusion tensor imaging at four months; and significantly improved motor and cognitive recovery in comparison to the other treatment groups. Markedly delayed, single dose treatment with CHPG significantly improves functional recovery and limits lesion progression after experimental traumatic brain injury, likely in part through actions at mGluR5 receptors that modulate neuroinflammation. Abstract Background Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss may continue for months or years after traumatic brain injury in association with chronic microglial activation. Recently we found that metabotropic glutamate receptor 5 (mGluR5) activation by ( RS )-2-chloro-5-hydroxyphenylglycine (CHPG) decreases microglial activation and release of associated pro-inflammatory factors in vitro , which is mediated in part through inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Here we examined whether delayed CHPG administration reduces chronic neuroinflammation and associated neurodegeneration after experimental traumatic brain injury in mice. Methods One month after controlled cortical impact traumatic brain injury, C57Bl/6 mice were randomly assigned to treatment with single dose intracerebroventricular CHPG, vehicle or CHPG plus a selective mGluR5 antagonist, 3-((2-Methyl-4-thiazolyl)ethynyl)pyridine. Lesion volume, white matter tract integrity and neurological recovery were assessed over the following three months. Results Traumatic brain injury resulted in mGluR5 expression in reactive microglia of the cortex and hippocampus at one month post-injury. Delayed CHPG treatment reduced expression of reactive microglia expressing NADPH oxidase subunits; decreased hippocampal neuronal loss; limited lesion progression, as measured by repeated T2-weighted magnetic resonance imaging (at one, two and three months) and white matter loss, as measured by high field ex vivo diffusion tensor imaging at four months; and significantly improved motor and cognitive recovery in comparison to the other treatment groups. Conclusion Markedly delayed, single dose treatment with CHPG significantly improves functional recovery and limits lesion progression after experimental traumatic brain injury, likely in part through actions at mGluR5 receptors that modulate neuroinflammation. Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss may continue for months or years after traumatic brain injury in association with chronic microglial activation. Recently we found that metabotropic glutamate receptor 5 (mGluR5) activation by (RS)-2-chloro-5-hydroxyphenylglycine (CHPG) decreases microglial activation and release of associated pro-inflammatory factors in vitro, which is mediated in part through inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Here we examined whether delayed CHPG administration reduces chronic neuroinflammation and associated neurodegeneration after experimental traumatic brain injury in mice. One month after controlled cortical impact traumatic brain injury, C57Bl/6 mice were randomly assigned to treatment with single dose intracerebroventricular CHPG, vehicle or CHPG plus a selective mGluR5 antagonist, 3-((2-Methyl-4-thiazolyl)ethynyl)pyridine. Lesion volume, white matter tract integrity and neurological recovery were assessed over the following three months. Traumatic brain injury resulted in mGluR5 expression in reactive microglia of the cortex and hippocampus at one month post-injury. Delayed CHPG treatment reduced expression of reactive microglia expressing NADPH oxidase subunits; decreased hippocampal neuronal loss; limited lesion progression, as measured by repeated T2-weighted magnetic resonance imaging (at one, two and three months) and white matter loss, as measured by high field ex vivo diffusion tensor imaging at four months; and significantly improved motor and cognitive recovery in comparison to the other treatment groups. Markedly delayed, single dose treatment with CHPG significantly improves functional recovery and limits lesion progression after experimental traumatic brain injury, likely in part through actions at mGluR5 receptors that modulate neuroinflammation. Background Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss may continue for months or years after traumatic brain injury in association with chronic microglial activation. Recently we found that metabotropic glutamate receptor 5 (mGluR5) activation by (RS)-2-chloro-5-hydroxyphenylglycine (CHPG) decreases microglial activation and release of associated pro-inflammatory factors in vitro, which is mediated in part through inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Here we examined whether delayed CHPG administration reduces chronic neuroinflammation and associated neurodegeneration after experimental traumatic brain injury in mice. Methods One month after controlled cortical impact traumatic brain injury, C57Bl/6 mice were randomly assigned to treatment with single dose intracerebroventricular CHPG, vehicle or CHPG plus a selective mGluR5 antagonist, 3-((2-Methyl-4-thiazolyl)ethynyl)pyridine. Lesion volume, white matter tract integrity and neurological recovery were assessed over the following three months. Results Traumatic brain injury resulted in mGluR5 expression in reactive microglia of the cortex and hippocampus at one month post-injury. Delayed CHPG treatment reduced expression of reactive microglia expressing NADPH oxidase subunits; decreased hippocampal neuronal loss; limited lesion progression, as measured by repeated T2-weighted magnetic resonance imaging (at one, two and three months) and white matter loss, as measured by high field ex vivo diffusion tensor imaging at four months; and significantly improved motor and cognitive recovery in comparison to the other treatment groups. Conclusion Markedly delayed, single dose treatment with CHPG significantly improves functional recovery and limits lesion progression after experimental traumatic brain injury, likely in part through actions at mGluR5 receptors that modulate neuroinflammation. Keywords: Traumatic brain injury, microglia, metabotropic glutamate receptor 5, delayed treatment, neuroprotection |
| ArticleNumber | 43 |
| Audience | Academic |
| Author | Loane, David J Zhang, Jiangyang Byrnes, Kimberly R Faden, Alan I Stoica, Bogdan A |
| AuthorAffiliation | 4 Department of Radiology, Johns Hopkins University, Baltimore, MD, USA 3 Department of Anesthesiology & Center for Shock, Trauma and Anesthesiology Research (STAR), National Study Center for Trauma and EMS, University of Maryland School of Medicine, Baltimore, MD, USA 2 Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD, USA 1 Department of Neuroscience, Georgetown University Medical Center, Washington, DC, USA |
| AuthorAffiliation_xml | – name: 4 Department of Radiology, Johns Hopkins University, Baltimore, MD, USA – name: 3 Department of Anesthesiology & Center for Shock, Trauma and Anesthesiology Research (STAR), National Study Center for Trauma and EMS, University of Maryland School of Medicine, Baltimore, MD, USA – name: 2 Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD, USA – name: 1 Department of Neuroscience, Georgetown University Medical Center, Washington, DC, USA |
| Author_xml | – sequence: 1 givenname: Kimberly R surname: Byrnes fullname: Byrnes, Kimberly R organization: Department of Neuroscience, Georgetown University Medical Center, Washington, DC, USA – sequence: 2 givenname: David J surname: Loane fullname: Loane, David J – sequence: 3 givenname: Bogdan A surname: Stoica fullname: Stoica, Bogdan A – sequence: 4 givenname: Jiangyang surname: Zhang fullname: Zhang, Jiangyang – sequence: 5 givenname: Alan I surname: Faden fullname: Faden, Alan I |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22373400$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1002/ana.21673 10.1097/00004728-199801000-00027 10.1097/00004728-199801000-00028 10.1016/j.it.2008.05.002 10.1007/s00401-001-0510-8 10.1002/glia.1106 10.1074/jbc.M806139200 10.1089/neu.2006.0205 10.1006/jmrb.1994.1037 10.1016/j.tips.2010.09.005 10.1002/1097-4547(20010101)63:1<90::AID-JNR11>3.0.CO;2-9 10.1016/0361-9230(94)90189-9 10.1523/JNEUROSCI.12-12-04846.1992 10.1097/00001756-200011090-00013 10.1002/glia.20295 10.1523/JNEUROSCI.3257-09.2009 10.1016/j.neuropharm.2010.10.022 10.1089/neu.1997.14.715 10.1097/CCM.0b013e3181921225 10.1016/j.cmpb.2005.08.004 10.1097/01.jnen.0000229241.28619.75 10.1038/nn1472 10.1016/j.nbd.2011.01.027 10.1016/j.nurt.2010.07.002 10.1016/j.pneurobio.2005.06.004 10.1016/j.expneurol.2005.10.020 10.1097/00019052-200212000-00008 10.1038/sj.cdd.4400678 10.1002/ana.22455 10.1038/nm.1940 10.1002/mrm.22426 10.1016/j.neuroscience.2009.05.070 10.1089/neu.1995.12.169 10.1074/jbc.M307657200 10.1016/j.forsciint.2004.06.027 10.1016/j.brainres.2008.07.094 10.1007/s00401-005-1010-z 10.1002/glia.21086 10.1016/S0079-6123(06)61009-1 10.1089/neu.1999.16.1023 10.1089/neu.2007.0377 10.1016/j.expneurol.2007.03.031 10.1089/neu.1998.15.599 10.1007/s12035-009-8077-9 10.1016/S0006-8993(01)03062-1 10.1126/science.1110647 10.1016/j.biocel.2004.06.010 10.1089/089771504322972031 10.1002/glia.20783 10.1016/j.nurt.2009.10.023 10.1073/pnas.0307850101 10.1523/JNEUROSCI.3647-07.2007 10.1002/mrm.1910390610 10.1038/jcbfm.2011.117 10.1016/j.neuroimage.2008.08.030 10.1016/j.nurt.2008.10.038 10.1093/brain/awn247 10.1016/j.neuroimage.2008.04.254 10.1038/nrn2038 10.1002/glia.10146 |
| ContentType | Journal Article |
| Copyright | COPYRIGHT 2012 BioMed Central Ltd. 2012 Byrnes et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright ©2012 Byrnes et al; licensee BioMed Central Ltd. 2012 Byrnes et al; licensee BioMed Central Ltd. |
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| References | 16081203 - Prog Neurobiol. 2005 Jun;76(2):77-98 18804539 - Neuroimage. 2009 Jan 1;44(1):1-8 18816644 - Glia. 2009 Apr 1;57(5):550-60 17518532 - J Neurotrauma. 2007 May;24(5):766-71 18599350 - Trends Immunol. 2008 Aug;29(8):357-65 15831717 - Science. 2005 May 27;308(5726):1314-8 9621916 - Magn Reson Med. 1998 Jun;39(6):928-34 12012093 - Acta Neuropathol. 2002 Jun;103(6):607-14 12379910 - Glia. 2002 Nov;40(2):232-9 16309676 - Exp Neurol. 2006 Feb;197(2):330-40 19104212 - Crit Care Med. 2009 Jan;37(1 Suppl):S129-35 10800080 - Cell Death Differ. 2000 May;7(5):470-6 18708034 - Brain Res. 2008 Oct 9;1234:183-97 20129492 - Neurotherapeutics. 2010 Jan;7(1):3-12 21895533 - J Neurotrauma. 2012 Mar 20;29(5):813-27 1464770 - J Neurosci. 1992 Dec;12(12):4846-53 16772871 - J Neuropathol Exp Neurol. 2006 May;65(5):478-88 9448780 - J Comput Assist Tomogr. 1998 Jan-Feb;22(1):153-65 8019776 - J Magn Reson B. 1994 Mar;103(3):247-54 15877231 - Acta Neuropathol. 2005 Jun;109(6):603-16 21829212 - J Cereb Blood Flow Metab. 2012 Jan;32(1):137-49 21125661 - Glia. 2011 Feb;59(2):188-99 19287391 - Nat Med. 2009 Apr;15(4):377-9 19864556 - J Neurosci. 2009 Oct 28;29(43):13435-44 12447109 - Curr Opin Neurol. 2002 Dec;15(6):707-12 10595819 - J Neurotrauma. 1999 Nov;16(11):1023-34 11095500 - Neuroreport. 2000 Nov 9;11(16):3461-5 11596125 - Glia. 2001 Nov;36(2):165-79 9726259 - J Neurotrauma. 1998 Aug;15(8):599-614 19490934 - Neuroscience. 2009 Sep 15;162(4):1339-50 21303700 - Neurobiol Dis. 2011 Jun;42(3):341-8 20577980 - Magn Reson Med. 2010 Jul;64(1):249-61 11169618 - J Neurosci Res. 2001 Jan 1;63(1):90-7 9448779 - J Comput Assist Tomogr. 1998 Jan-Feb;22(1):139-52 17618974 - Prog Brain Res. 2007;161:125-41 17180163 - Nat Rev Neurosci. 2007 Jan;8(1):57-69 19364772 - J Biol Chem. 2009 Jun 5;284(23):15629-39 15115599 - J Neurotrauma. 2004 Mar;21(3):239-50 15542269 - Forensic Sci Int. 2004 Dec 16;146(2-3):97-104 21036182 - Neuropharmacology. 2011 Jun;60(7-8):1017-41 16413083 - Comput Methods Programs Biomed. 2006 Feb;81(2):106-16 19110202 - Neurotherapeutics. 2009 Jan;6(1):94-107 15381143 - Int J Biochem Cell Biol. 2005 Jan;37(1):17-21 9383090 - J Neurotrauma. 1997 Oct;14(10):715-27 18952679 - Brain. 2008 Dec;131(Pt 12):3209-21 19670441 - Ann Neurol. 2009 Jul;66(1):63-74 18001202 - J Neurotrauma. 2007 Nov;24(11):1719-42 18556217 - Neuroimage. 2008 Aug 15;42(2):503-14 11743947 - Brain Res. 2001 Dec 20;922(2):173-9 15895084 - Nat Neurosci. 2005 Jun;8(6):752-8 20880501 - Neurotherapeutics. 2010 Oct;7(4):366-77 19629762 - Mol Neurobiol. 2009 Oct;40(2):139-56 17978027 - J Neurosci. 2007 Oct 31;27(44):11869-76 15136737 - Proc Natl Acad Sci U S A. 2004 May 18;101(20):7751-6 16345062 - Glia. 2006 Mar;53(4):420-33 21710619 - Ann Neurol. 2011 Sep;70(3):374-83 8193937 - Brain Res Bull. 1994;34(1):73-8 17521631 - Exp Neurol. 2007 Jul;206(1):59-69 14578353 - J Biol Chem. 2004 Jan 9;279(2):1415-21 21035878 - Trends Pharmacol Sci. 2010 Dec;31(12):596-604 7629863 - J Neurotrauma. 1995 Apr;12(2):169-78 W Deng (532_CR52_532) 2004; 101 K Nagamoto-Combs (532_CR10_532) 2007; 24 DH Smith (532_CR61_532) 1995; 12 P Eikelenboom (532_CR46_532) 2002; 40 DL Brody (532_CR33_532) 2006; 197 SN Niogi (532_CR59_532) 2008; 131 WL Maxwell (532_CR13_532) 2006; 65 DJ Loane (532_CR1_532) 2010; 31 WL Bao (532_CR24_532) 2001; 922 RP Woods (532_CR30_532) 1998; 22 KR Byrnes (532_CR20_532) 2009; 66 J Drouin-Ouellet (532_CR40_532) 2011; 59 SM Gentleman (532_CR11_532) 2004; 146 F Vilhardt (532_CR42_532) 2005; 37 M Aggarwal (532_CR29_532) 2009; 162 KR Byrnes (532_CR49_532) 2009; 6 BA Stoica (532_CR54_532) 2010; 7 MA Lynch (532_CR43_532) 2009; 40 Z Soltys (532_CR34_532) 2001; 63 KR Byrnes (532_CR16_532) 2006; 53 KM Frick (532_CR32_532) 2000; 11 H Jiang (532_CR28_532) 2006; 81 KA Kigerl (532_CR47_532) 2009; 29 BB Bendlin (532_CR15_532) 2008; 42 PJ Basser (532_CR27_532) 1998; 39 DJ Loane (532_CR3_532) 2010; 7 X Zhan (532_CR37_532) 2008; 1234 H Wang (532_CR45_532) 2007; 206 L Qin (532_CR17_532) 2004; 279 DH Smith (532_CR12_532) 1997; 14 HM Gao (532_CR18_532) 2008; 29 ML Block (532_CR5_532) 2007; 8 A Sidaros (532_CR57_532) 2009; 44 SV Kabadi (532_CR35_532) 2011; 32 PJ Basser (532_CR26_532) 1994; 103 DJ Loane (532_CR19_532) 2009; 284 F Aloisi (532_CR6_532) 2001; 36 S Wilson (532_CR8_532) 2004; 21 DK Menon (532_CR53_532) 2009; 37 DJ Loane (532_CR23_532) 2009; 15 ML Block (532_CR7_532) 2005; 76 KR Byrnes (532_CR21_532) 2009; 57 HM Bramlett (532_CR14_532) 2002; 103 AI Faden (532_CR55_532) 2002; 15 SV Kabadi (532_CR44_532) 2012 A Nimmerjahn (532_CR41_532) 2005; 308 M Nonaka (532_CR38_532) 1999; 16 GB Fox (532_CR22_532) 1998; 15 DH Lowenstein (532_CR60_532) 1992; 12 H Chen (532_CR48_532) 2011; 42 JW Allen (532_CR51_532) 2000; 7 F Nicoletti (532_CR50_532) 2010; 60 AC Rodriguez-Paez (532_CR39_532) 2005; 109 RP Woods (532_CR31_532) 1998; 22 HM Bramlett (532_CR2_532) 2007; 161 AF Ramlackhansingh (532_CR9_532) 2011; 70 M Aggarwal (532_CR25_532) 2010; 64 CL Mac Donald (532_CR58_532) 2007; 27 D Davalos (532_CR4_532) 2005; 8 E Davis (532_CR36_532) 1994; 34 MA Trivedi (532_CR56_532) 2007; 24 |
| References_xml | – volume: 66 start-page: 63 year: 2009 ident: 532_CR20_532 publication-title: Ann Neurol doi: 10.1002/ana.21673 contributor: fullname: KR Byrnes – volume: 22 start-page: 139 year: 1998 ident: 532_CR30_532 publication-title: J Comput Assist Tomogr doi: 10.1097/00004728-199801000-00027 contributor: fullname: RP Woods – volume-title: J Neurotrauma year: 2012 ident: 532_CR44_532 contributor: fullname: SV Kabadi – volume: 22 start-page: 153 year: 1998 ident: 532_CR31_532 publication-title: J Comput Assist Tomogr doi: 10.1097/00004728-199801000-00028 contributor: fullname: RP Woods – volume: 29 start-page: 357 year: 2008 ident: 532_CR18_532 publication-title: Trends Immunol doi: 10.1016/j.it.2008.05.002 contributor: fullname: HM Gao – volume: 103 start-page: 607 year: 2002 ident: 532_CR14_532 publication-title: Acta Neuropathol doi: 10.1007/s00401-001-0510-8 contributor: fullname: HM Bramlett – volume: 36 start-page: 165 year: 2001 ident: 532_CR6_532 publication-title: Glia doi: 10.1002/glia.1106 contributor: fullname: F Aloisi – volume: 284 start-page: 15629 year: 2009 ident: 532_CR19_532 publication-title: J Biol Chem doi: 10.1074/jbc.M806139200 contributor: fullname: DJ Loane – volume: 24 start-page: 766 year: 2007 ident: 532_CR56_532 publication-title: J Neurotrauma doi: 10.1089/neu.2006.0205 contributor: fullname: MA Trivedi – volume: 103 start-page: 247 year: 1994 ident: 532_CR26_532 publication-title: J Magn Reson B doi: 10.1006/jmrb.1994.1037 contributor: fullname: PJ Basser – volume: 31 start-page: 596 year: 2010 ident: 532_CR1_532 publication-title: Trends Pharmacol Sci doi: 10.1016/j.tips.2010.09.005 contributor: fullname: DJ Loane – volume: 63 start-page: 90 year: 2001 ident: 532_CR34_532 publication-title: J Neurosci Res doi: 10.1002/1097-4547(20010101)63:1<90::AID-JNR11>3.0.CO;2-9 contributor: fullname: Z Soltys – volume: 34 start-page: 73 year: 1994 ident: 532_CR36_532 publication-title: Brain Res Bull doi: 10.1016/0361-9230(94)90189-9 contributor: fullname: E Davis – volume: 12 start-page: 4846 year: 1992 ident: 532_CR60_532 publication-title: J Neurosci doi: 10.1523/JNEUROSCI.12-12-04846.1992 contributor: fullname: DH Lowenstein – volume: 11 start-page: 3461 year: 2000 ident: 532_CR32_532 publication-title: NeuroReport doi: 10.1097/00001756-200011090-00013 contributor: fullname: KM Frick – volume: 53 start-page: 420 year: 2006 ident: 532_CR16_532 publication-title: Glia doi: 10.1002/glia.20295 contributor: fullname: KR Byrnes – volume: 29 start-page: 13435 year: 2009 ident: 532_CR47_532 publication-title: J Neurosci doi: 10.1523/JNEUROSCI.3257-09.2009 contributor: fullname: KA Kigerl – volume: 60 start-page: 1017 year: 2010 ident: 532_CR50_532 publication-title: Neuropharmacology doi: 10.1016/j.neuropharm.2010.10.022 contributor: fullname: F Nicoletti – volume: 14 start-page: 715 year: 1997 ident: 532_CR12_532 publication-title: J Neurotrauma doi: 10.1089/neu.1997.14.715 contributor: fullname: DH Smith – volume: 37 start-page: S129-135 year: 2009 ident: 532_CR53_532 publication-title: Crit Care Med doi: 10.1097/CCM.0b013e3181921225 contributor: fullname: DK Menon – volume: 81 start-page: 106 year: 2006 ident: 532_CR28_532 publication-title: Comput Methods Programs Biomed doi: 10.1016/j.cmpb.2005.08.004 contributor: fullname: H Jiang – volume: 65 start-page: 478 year: 2006 ident: 532_CR13_532 publication-title: J Neuropathol Exp Neurol doi: 10.1097/01.jnen.0000229241.28619.75 contributor: fullname: WL Maxwell – volume: 8 start-page: 752 year: 2005 ident: 532_CR4_532 publication-title: Nat Neurosci doi: 10.1038/nn1472 contributor: fullname: D Davalos – volume: 42 start-page: 341 year: 2011 ident: 532_CR48_532 publication-title: Neurobiol Dis doi: 10.1016/j.nbd.2011.01.027 contributor: fullname: H Chen – volume: 7 start-page: 366 year: 2010 ident: 532_CR3_532 publication-title: Neurotherapeutics doi: 10.1016/j.nurt.2010.07.002 contributor: fullname: DJ Loane – volume: 76 start-page: 77 year: 2005 ident: 532_CR7_532 publication-title: Prog Neurobiol doi: 10.1016/j.pneurobio.2005.06.004 contributor: fullname: ML Block – volume: 197 start-page: 330 year: 2006 ident: 532_CR33_532 publication-title: Exp Neurol doi: 10.1016/j.expneurol.2005.10.020 contributor: fullname: DL Brody – volume: 15 start-page: 707 year: 2002 ident: 532_CR55_532 publication-title: Curr Opin Neurol doi: 10.1097/00019052-200212000-00008 contributor: fullname: AI Faden – volume: 7 start-page: 470 year: 2000 ident: 532_CR51_532 publication-title: Cell Death Differ doi: 10.1038/sj.cdd.4400678 contributor: fullname: JW Allen – volume: 70 start-page: 374 year: 2011 ident: 532_CR9_532 publication-title: Ann Neurol doi: 10.1002/ana.22455 contributor: fullname: AF Ramlackhansingh – volume: 15 start-page: 377 year: 2009 ident: 532_CR23_532 publication-title: Nat Med doi: 10.1038/nm.1940 contributor: fullname: DJ Loane – volume: 64 start-page: 249 year: 2010 ident: 532_CR25_532 publication-title: Magn Reson Med doi: 10.1002/mrm.22426 contributor: fullname: M Aggarwal – volume: 162 start-page: 1339 year: 2009 ident: 532_CR29_532 publication-title: Neuroscience doi: 10.1016/j.neuroscience.2009.05.070 contributor: fullname: M Aggarwal – volume: 12 start-page: 169 year: 1995 ident: 532_CR61_532 publication-title: J Neurotrauma doi: 10.1089/neu.1995.12.169 contributor: fullname: DH Smith – volume: 279 start-page: 1415 year: 2004 ident: 532_CR17_532 publication-title: J Biol Chem doi: 10.1074/jbc.M307657200 contributor: fullname: L Qin – volume: 146 start-page: 97 year: 2004 ident: 532_CR11_532 publication-title: Forensic Sci Int doi: 10.1016/j.forsciint.2004.06.027 contributor: fullname: SM Gentleman – volume: 1234 start-page: 184 year: 2008 ident: 532_CR37_532 publication-title: Brain Res doi: 10.1016/j.brainres.2008.07.094 contributor: fullname: X Zhan – volume: 109 start-page: 603 year: 2005 ident: 532_CR39_532 publication-title: Acta Neuropathol doi: 10.1007/s00401-005-1010-z contributor: fullname: AC Rodriguez-Paez – volume: 59 start-page: 188 year: 2011 ident: 532_CR40_532 publication-title: Glia doi: 10.1002/glia.21086 contributor: fullname: J Drouin-Ouellet – volume: 161 start-page: 125 year: 2007 ident: 532_CR2_532 publication-title: Prog Brain Res doi: 10.1016/S0079-6123(06)61009-1 contributor: fullname: HM Bramlett – volume: 16 start-page: 1023 year: 1999 ident: 532_CR38_532 publication-title: J Neurotrauma doi: 10.1089/neu.1999.16.1023 contributor: fullname: M Nonaka – volume: 24 start-page: 1719 year: 2007 ident: 532_CR10_532 publication-title: J Neurotrauma doi: 10.1089/neu.2007.0377 contributor: fullname: K Nagamoto-Combs – volume: 206 start-page: 59 year: 2007 ident: 532_CR45_532 publication-title: Exp Neurol doi: 10.1016/j.expneurol.2007.03.031 contributor: fullname: H Wang – volume: 15 start-page: 599 year: 1998 ident: 532_CR22_532 publication-title: J Neurotrauma doi: 10.1089/neu.1998.15.599 contributor: fullname: GB Fox – volume: 40 start-page: 139 year: 2009 ident: 532_CR43_532 publication-title: Mol Neurobiol doi: 10.1007/s12035-009-8077-9 contributor: fullname: MA Lynch – volume: 922 start-page: 173 year: 2001 ident: 532_CR24_532 publication-title: Brain Res doi: 10.1016/S0006-8993(01)03062-1 contributor: fullname: WL Bao – volume: 308 start-page: 1314 year: 2005 ident: 532_CR41_532 publication-title: Science doi: 10.1126/science.1110647 contributor: fullname: A Nimmerjahn – volume: 37 start-page: 17 year: 2005 ident: 532_CR42_532 publication-title: Int J Biochem Cell Biol doi: 10.1016/j.biocel.2004.06.010 contributor: fullname: F Vilhardt – volume: 21 start-page: 239 year: 2004 ident: 532_CR8_532 publication-title: J Neurotrauma doi: 10.1089/089771504322972031 contributor: fullname: S Wilson – volume: 57 start-page: 550 year: 2009 ident: 532_CR21_532 publication-title: Glia doi: 10.1002/glia.20783 contributor: fullname: KR Byrnes – volume: 7 start-page: 3 year: 2010 ident: 532_CR54_532 publication-title: Neurotherapeutics doi: 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| Snippet | Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss may continue for... Abstract Background Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss... Background Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss may... Doc number: 43 Abstract Background: Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest... BACKGROUND: Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss may... Abstract Background Traumatic brain injury initiates biochemical processes that lead to secondary neurodegeneration. Imaging studies suggest that tissue loss... |
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| SubjectTerms | Anatomy & physiology Anesthesiology Animal cognition Animals Apoptosis Brain Brain damage Brain injuries Brain Injuries - complications Calcium-Binding Proteins - metabolism Cell receptors Cognition Disorders - etiology Degeneration delayed treatment Diffusion Tensor Imaging Disease Models, Animal Ectodysplasins - metabolism Encephalitis - drug therapy Encephalitis - etiology Encephalitis - metabolism Excitatory Amino Acid Agonists - therapeutic use Excitatory Amino Acid Antagonists - pharmacology Gene expression Gene Expression Regulation - drug effects Glutamate Glycine - analogs & derivatives Glycine - therapeutic use Health sciences Hippocampus - pathology House mouse Injuries Magnetic Resonance Imaging Male metabotropic glutamate receptor 5 Mice Mice, Inbred C57BL Microfilament Proteins - metabolism microglia Microglia - drug effects Microglia - metabolism Motion detectors Movement Disorders - etiology Nervous system Neurodegeneration Neurodegenerative Diseases - drug therapy Neurodegenerative Diseases - etiology Neurodegenerative Diseases - metabolism Neurons Neurons - pathology neuroprotection Neurosciences Niacinamide Nitric oxide Oxidases Phenylacetates - therapeutic use Phosphates Physiological aspects Purines Pyridine Pyridines - pharmacology Receptor, Metabotropic Glutamate 5 Receptors, Immunologic - metabolism Receptors, Metabotropic Glutamate - metabolism Recovery of Function - drug effects Rodents Statistics, Nonparametric Studies Thiazoles - pharmacology Time Factors Traumatic brain injury |
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| Title | Delayed mGluR5 activation limits neuroinflammation and neurodegeneration after traumatic brain injury |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/22373400 https://www.proquest.com/docview/929146598/abstract/ http://dx.doi.org/10.1186/1742-2094-9-43 https://pubmed.ncbi.nlm.nih.gov/PMC3308916 https://doaj.org/article/6df063bcb1ed4e939078b16a28ed58d7 |
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