NMDA receptor subunits have different roles in NMDA-induced neurotoxicity in the retina
Loss of retinal ganglion cells (RGCs) is a hallmark of various retinal diseases including glaucoma, retinal ischemia, and diabetic retinopathy. N-methyl-D-aspartate (NMDA)-type glutamate receptor (NMDAR)-mediated excitotoxicity is thought to be an important contributor to RGC death in these diseases...
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| Veröffentlicht in: | Molecular brain 2013-07, Vol.6 (1), p.34-34 |
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| creator | Bai, Ning Aida, Tomomi Yanagisawa, Michiko Katou, Sayaka Sakimura, Kenji Mishina, Masayoshi Tanaka, Kohichi |
| description | Loss of retinal ganglion cells (RGCs) is a hallmark of various retinal diseases including glaucoma, retinal ischemia, and diabetic retinopathy. N-methyl-D-aspartate (NMDA)-type glutamate receptor (NMDAR)-mediated excitotoxicity is thought to be an important contributor to RGC death in these diseases. Native NMDARs are heterotetramers that consist of GluN1 and GluN2 subunits, and GluN2 subunits (GluN2A-D) are major determinants of the pharmacological and biophysical properties of NMDARs. All NMDAR subunits are expressed in RGCs in the retina. However, the relative contribution of the different GluN2 subunits to RGC death by excitotoxicity remains unclear.
GluN2B- and GluN2D-deficiency protected RGCs from NMDA-induced excitotoxic retinal cell death. Pharmacological inhibition of the GluN2B subunit attenuated RGC loss in glutamate aspartate transporter deficient mice.
Our data suggest that GluN2B- and GluN2D-containing NMDARs play a critical role in NMDA-induced excitotoxic retinal cell death and RGC degeneration in glutamate aspartate transporter deficient mice. Inhibition of GluN2B and GluN2D activity is a potential therapeutic strategy for the treatment of several retinal diseases. |
| doi_str_mv | 10.1186/1756-6606-6-34 |
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GluN2B- and GluN2D-deficiency protected RGCs from NMDA-induced excitotoxic retinal cell death. Pharmacological inhibition of the GluN2B subunit attenuated RGC loss in glutamate aspartate transporter deficient mice.
Our data suggest that GluN2B- and GluN2D-containing NMDARs play a critical role in NMDA-induced excitotoxic retinal cell death and RGC degeneration in glutamate aspartate transporter deficient mice. Inhibition of GluN2B and GluN2D activity is a potential therapeutic strategy for the treatment of several retinal diseases.</description><identifier>ISSN: 1756-6606</identifier><identifier>EISSN: 1756-6606</identifier><identifier>DOI: 10.1186/1756-6606-6-34</identifier><identifier>PMID: 23902942</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Animals ; Apoptosis ; Brain research ; Cell Death - drug effects ; Diabetic retinopathy ; Excitatory Amino Acid Transporter 1 - deficiency ; Excitatory Amino Acid Transporter 1 - metabolism ; Experiments ; Gene Deletion ; In Situ Nick-End Labeling ; Ischemia ; Isoquinolines - pharmacology ; Methyl aspartate ; Mice ; N-Methylaspartate - toxicity ; Neural receptors ; Neurosciences ; Neurotoxicity syndromes ; Neurotoxins - toxicity ; Permeability ; Physiological aspects ; Polymerase chain reaction ; Protein Subunits - antagonists & inhibitors ; Protein Subunits - metabolism ; Proteins ; Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors ; Receptors, N-Methyl-D-Aspartate - metabolism ; Retina ; Retina - drug effects ; Retina - metabolism ; Retina - pathology ; Retinal diseases ; Rodents ; Science</subject><ispartof>Molecular brain, 2013-07, Vol.6 (1), p.34-34</ispartof><rights>COPYRIGHT 2013 BioMed Central Ltd.</rights><rights>2013 Bai 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.</rights><rights>Copyright © 2013 Bai et al.; licensee BioMed Central Ltd. 2013 Bai et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b642t-5257ee96a7de5646f99693daf4e4863d55f2c8e7f55068ce268ff58378f398033</citedby><cites>FETCH-LOGICAL-b642t-5257ee96a7de5646f99693daf4e4863d55f2c8e7f55068ce268ff58378f398033</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3733768/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3733768/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23902942$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bai, Ning</creatorcontrib><creatorcontrib>Aida, Tomomi</creatorcontrib><creatorcontrib>Yanagisawa, Michiko</creatorcontrib><creatorcontrib>Katou, Sayaka</creatorcontrib><creatorcontrib>Sakimura, Kenji</creatorcontrib><creatorcontrib>Mishina, Masayoshi</creatorcontrib><creatorcontrib>Tanaka, Kohichi</creatorcontrib><title>NMDA receptor subunits have different roles in NMDA-induced neurotoxicity in the retina</title><title>Molecular brain</title><addtitle>Mol Brain</addtitle><description>Loss of retinal ganglion cells (RGCs) is a hallmark of various retinal diseases including glaucoma, retinal ischemia, and diabetic retinopathy. N-methyl-D-aspartate (NMDA)-type glutamate receptor (NMDAR)-mediated excitotoxicity is thought to be an important contributor to RGC death in these diseases. Native NMDARs are heterotetramers that consist of GluN1 and GluN2 subunits, and GluN2 subunits (GluN2A-D) are major determinants of the pharmacological and biophysical properties of NMDARs. All NMDAR subunits are expressed in RGCs in the retina. However, the relative contribution of the different GluN2 subunits to RGC death by excitotoxicity remains unclear.
GluN2B- and GluN2D-deficiency protected RGCs from NMDA-induced excitotoxic retinal cell death. Pharmacological inhibition of the GluN2B subunit attenuated RGC loss in glutamate aspartate transporter deficient mice.
Our data suggest that GluN2B- and GluN2D-containing NMDARs play a critical role in NMDA-induced excitotoxic retinal cell death and RGC degeneration in glutamate aspartate transporter deficient mice. Inhibition of GluN2B and GluN2D activity is a potential therapeutic strategy for the treatment of several retinal diseases.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Brain research</subject><subject>Cell Death - drug effects</subject><subject>Diabetic retinopathy</subject><subject>Excitatory Amino Acid Transporter 1 - deficiency</subject><subject>Excitatory Amino Acid Transporter 1 - metabolism</subject><subject>Experiments</subject><subject>Gene Deletion</subject><subject>In Situ Nick-End Labeling</subject><subject>Ischemia</subject><subject>Isoquinolines - pharmacology</subject><subject>Methyl aspartate</subject><subject>Mice</subject><subject>N-Methylaspartate - toxicity</subject><subject>Neural receptors</subject><subject>Neurosciences</subject><subject>Neurotoxicity syndromes</subject><subject>Neurotoxins - toxicity</subject><subject>Permeability</subject><subject>Physiological aspects</subject><subject>Polymerase chain reaction</subject><subject>Protein Subunits - antagonists & inhibitors</subject><subject>Protein Subunits - metabolism</subject><subject>Proteins</subject><subject>Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors</subject><subject>Receptors, N-Methyl-D-Aspartate - metabolism</subject><subject>Retina</subject><subject>Retina - drug effects</subject><subject>Retina - metabolism</subject><subject>Retina - pathology</subject><subject>Retinal diseases</subject><subject>Rodents</subject><subject>Science</subject><issn>1756-6606</issn><issn>1756-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kstrFTEUxoNYbK1uXcqAGzfT5jF5bYRL66PQ6kZxGXIzJ70pM8k1mSn2vzdD67XVSiAJ53z55ZyPg9Argo8IUeKYSC5aIXDdWtY9QQe7wNN79330vJQrjAUVhD9D-5RpTHVHD9D3zxenqyaDg-2UclPm9RzDVJqNvYamD95Dhjg1OQ1QmhCbRd6G2M8O-ibCnNOUfgYXppslO22gsqYQ7Qu05-1Q4OXdeYi-fXj_9eRTe_7l49nJ6rxdi45OLadcAmhhZQ9cdMJrLTTrre-gU4L1nHvqFEjPORbKARXKe66YVJ5phRk7RO9uudt5PULvarHZDmabw2jzjUk2mIeZGDbmMl0bJhmTQlXA6hawDuk_gIcZl0azGGsWY40wrKuMt3dF5PRjhjKZMRQHw2AjpLkY0lGJCeFaVumbv6RXac6xWlRVRGOtFRN_VJd2ABOiT_Vrt0DNirNOCk3owjp6RFVXD2NwKYIPNf7YA5dTKRn8rk2CzTJO_zb2-r67O_nv-WG_AFw5xC0</recordid><startdate>20130731</startdate><enddate>20130731</enddate><creator>Bai, Ning</creator><creator>Aida, Tomomi</creator><creator>Yanagisawa, Michiko</creator><creator>Katou, Sayaka</creator><creator>Sakimura, Kenji</creator><creator>Mishina, Masayoshi</creator><creator>Tanaka, Kohichi</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20130731</creationdate><title>NMDA receptor subunits have different roles in NMDA-induced neurotoxicity in the retina</title><author>Bai, Ning ; 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N-methyl-D-aspartate (NMDA)-type glutamate receptor (NMDAR)-mediated excitotoxicity is thought to be an important contributor to RGC death in these diseases. Native NMDARs are heterotetramers that consist of GluN1 and GluN2 subunits, and GluN2 subunits (GluN2A-D) are major determinants of the pharmacological and biophysical properties of NMDARs. All NMDAR subunits are expressed in RGCs in the retina. However, the relative contribution of the different GluN2 subunits to RGC death by excitotoxicity remains unclear.
GluN2B- and GluN2D-deficiency protected RGCs from NMDA-induced excitotoxic retinal cell death. Pharmacological inhibition of the GluN2B subunit attenuated RGC loss in glutamate aspartate transporter deficient mice.
Our data suggest that GluN2B- and GluN2D-containing NMDARs play a critical role in NMDA-induced excitotoxic retinal cell death and RGC degeneration in glutamate aspartate transporter deficient mice. Inhibition of GluN2B and GluN2D activity is a potential therapeutic strategy for the treatment of several retinal diseases.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>23902942</pmid><doi>10.1186/1756-6606-6-34</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apoptosis Brain research Cell Death - drug effects Diabetic retinopathy Excitatory Amino Acid Transporter 1 - deficiency Excitatory Amino Acid Transporter 1 - metabolism Experiments Gene Deletion In Situ Nick-End Labeling Ischemia Isoquinolines - pharmacology Methyl aspartate Mice N-Methylaspartate - toxicity Neural receptors Neurosciences Neurotoxicity syndromes Neurotoxins - toxicity Permeability Physiological aspects Polymerase chain reaction Protein Subunits - antagonists & inhibitors Protein Subunits - metabolism Proteins Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors Receptors, N-Methyl-D-Aspartate - metabolism Retina Retina - drug effects Retina - metabolism Retina - pathology Retinal diseases Rodents Science |
| title | NMDA receptor subunits have different roles in NMDA-induced neurotoxicity in the retina |
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