Memantine abrogates neurological deficits, but not CNS inflammation, in Lewis rat experimental autoimmune encephalomyelitis
Memantine, a clinically employed drug with N-methyl- d-aspartate (NMDA) receptor antagonistic effects, dose-dependently ameliorates neurological deficits in Lewis rat experimental autoimmune encephalomyelitis (EAE). Interestingly, this therapeutic effect was not due to dampened CNS inflammation, as...
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| Veröffentlicht in: | Journal of the neurological sciences 1996-05, Vol.137 (2), p.89-96 |
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| container_title | Journal of the neurological sciences |
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| creator | Wallström, Erik Diener, Per Ljungdahl, Åke Khademi, Mohsen Nilsson, Carl-Gustaf Olsson, Tomas |
| description | Memantine, a clinically employed drug with
N-methyl-
d-aspartate (NMDA) receptor antagonistic effects, dose-dependently ameliorates neurological deficits in Lewis rat experimental autoimmune encephalomyelitis (EAE). Interestingly, this therapeutic effect was not due to dampened CNS inflammation, as assessed by immunohistochemical evaluation of spinal cord tissue. Furthermore, numbers of interferon gamma (IFNγ) mRNA expressing cells were not decreased, as assessed by in situ hybridization. Systemic immunity in terms of numbers of IFNγ secreting cells in response to immunodominant myelin basic protein (MBP) peptides ex vivo was not reduced, and non-toxic doses of memantine did not affect lymphocyte proliferation or IFNγ secretion in vitro. Considering these findings, we hypothesize that effector mechanisms responsible for reversible neurological deficits in EAE may involve NMDA receptors, and this highlights neurons as targets during autoimmune neuroinflammation. |
| doi_str_mv | 10.1016/0022-510X(95)00339-4 |
| format | Article |
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N-methyl-
d-aspartate (NMDA) receptor antagonistic effects, dose-dependently ameliorates neurological deficits in Lewis rat experimental autoimmune encephalomyelitis (EAE). Interestingly, this therapeutic effect was not due to dampened CNS inflammation, as assessed by immunohistochemical evaluation of spinal cord tissue. Furthermore, numbers of interferon gamma (IFNγ) mRNA expressing cells were not decreased, as assessed by in situ hybridization. Systemic immunity in terms of numbers of IFNγ secreting cells in response to immunodominant myelin basic protein (MBP) peptides ex vivo was not reduced, and non-toxic doses of memantine did not affect lymphocyte proliferation or IFNγ secretion in vitro. Considering these findings, we hypothesize that effector mechanisms responsible for reversible neurological deficits in EAE may involve NMDA receptors, and this highlights neurons as targets during autoimmune neuroinflammation.</description><identifier>ISSN: 0022-510X</identifier><identifier>EISSN: 1878-5883</identifier><identifier>DOI: 10.1016/0022-510X(95)00339-4</identifier><identifier>PMID: 8782160</identifier><identifier>CODEN: JNSCAG</identifier><language>eng</language><publisher>Shannon: Elsevier B.V</publisher><subject>Animals ; Anticonvulsants. Antiepileptics. Antiparkinson agents ; Biological and medical sciences ; Cell Division - drug effects ; Central Nervous System Diseases - drug therapy ; Dose-Response Relationship, Drug ; Encephalomyelitis, Autoimmune, Experimental - drug therapy ; Excitatory Amino Acid Antagonists - therapeutic use ; Experimental autoimmune encephalomyelitis (EAE) ; Immunohistochemistry ; Interferon gamma (IFNγ) ; Interferon-gamma - biosynthesis ; Interferon-gamma - metabolism ; Interferon-gamma - physiology ; Male ; Medical sciences ; Medicin och hälsovetenskap ; Memantine ; Memantine - therapeutic use ; Myelin basic protein (MBP) ; Myelin Basic Protein - metabolism ; N-methyl- d-aspartate (NMDA) receptor ; Neurological deficit ; Neuropharmacology ; Pharmacology. Drug treatments ; Rats ; Rats, Inbred Lew ; Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors ; RNA, Messenger - analysis ; Spinal Cord - chemistry ; T-Lymphocytes - immunology</subject><ispartof>Journal of the neurological sciences, 1996-05, Vol.137 (2), p.89-96</ispartof><rights>1996</rights><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-b7e3a1b093ca9bcfdc89f1daaec230265ae36c58dc2bc72f9a4826fec6963eda3</citedby><cites>FETCH-LOGICAL-c503t-b7e3a1b093ca9bcfdc89f1daaec230265ae36c58dc2bc72f9a4826fec6963eda3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0022-510X(95)00339-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3122722$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8782160$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:1943074$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Wallström, Erik</creatorcontrib><creatorcontrib>Diener, Per</creatorcontrib><creatorcontrib>Ljungdahl, Åke</creatorcontrib><creatorcontrib>Khademi, Mohsen</creatorcontrib><creatorcontrib>Nilsson, Carl-Gustaf</creatorcontrib><creatorcontrib>Olsson, Tomas</creatorcontrib><title>Memantine abrogates neurological deficits, but not CNS inflammation, in Lewis rat experimental autoimmune encephalomyelitis</title><title>Journal of the neurological sciences</title><addtitle>J Neurol Sci</addtitle><description>Memantine, a clinically employed drug with
N-methyl-
d-aspartate (NMDA) receptor antagonistic effects, dose-dependently ameliorates neurological deficits in Lewis rat experimental autoimmune encephalomyelitis (EAE). Interestingly, this therapeutic effect was not due to dampened CNS inflammation, as assessed by immunohistochemical evaluation of spinal cord tissue. Furthermore, numbers of interferon gamma (IFNγ) mRNA expressing cells were not decreased, as assessed by in situ hybridization. Systemic immunity in terms of numbers of IFNγ secreting cells in response to immunodominant myelin basic protein (MBP) peptides ex vivo was not reduced, and non-toxic doses of memantine did not affect lymphocyte proliferation or IFNγ secretion in vitro. Considering these findings, we hypothesize that effector mechanisms responsible for reversible neurological deficits in EAE may involve NMDA receptors, and this highlights neurons as targets during autoimmune neuroinflammation.</description><subject>Animals</subject><subject>Anticonvulsants. Antiepileptics. Antiparkinson agents</subject><subject>Biological and medical sciences</subject><subject>Cell Division - drug effects</subject><subject>Central Nervous System Diseases - drug therapy</subject><subject>Dose-Response Relationship, Drug</subject><subject>Encephalomyelitis, Autoimmune, Experimental - drug therapy</subject><subject>Excitatory Amino Acid Antagonists - therapeutic use</subject><subject>Experimental autoimmune encephalomyelitis (EAE)</subject><subject>Immunohistochemistry</subject><subject>Interferon gamma (IFNγ)</subject><subject>Interferon-gamma - biosynthesis</subject><subject>Interferon-gamma - metabolism</subject><subject>Interferon-gamma - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicin och hälsovetenskap</subject><subject>Memantine</subject><subject>Memantine - therapeutic use</subject><subject>Myelin basic protein (MBP)</subject><subject>Myelin Basic Protein - metabolism</subject><subject>N-methyl- d-aspartate (NMDA) receptor</subject><subject>Neurological deficit</subject><subject>Neuropharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors</subject><subject>RNA, Messenger - analysis</subject><subject>Spinal Cord - chemistry</subject><subject>T-Lymphocytes - immunology</subject><issn>0022-510X</issn><issn>1878-5883</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcuO1DAQRS0EGnoG_gAkLxACaQJ-5GFvkFBreEgNLACJnVVxKoMhiYPtMIz4eRy6aVawsl117q2SLyH3OHvCGa-fMiZEUXH26ZGuHjMmpS7KG2TDVaOKSil5k2yOyG1yGuMXxlitlD4hJ5kRvGYb8vMNjjAlNyGFNvhLSBjphEvwg790FgbaYe-sS_Gctkuik090-_Y9dVM_wDhCcn46zy-6wysXaYBE8ceMwY04payGJXk3jkv2x8ni_BkGP17j4JKLd8itHoaIdw_nGfn44uLD9lWxe_fy9fb5rrAVk6loG5TAW6alBd3avrNK97wDQCskE3UFKGtbqc6K1jai11AqUfdoa11L7ECekWLvG69wXloz5-0gXBsPzhxKX_MNTVkyLVTmm3_yc_DdX9EfIdelZE2ZlQ_3yox9WzAmM7pocRhgQr9EwytVy6pZR5R70AYfY8D-OIQzs6Zr1ujMGp3Rlfmdrln97x_8l3bE7ig6xJn7Dw59iDm7PsBkXTxikgvRCJGxZ3sM869_dxhMtG6Np3MBbTKdd__f4xe0icZO</recordid><startdate>19960501</startdate><enddate>19960501</enddate><creator>Wallström, Erik</creator><creator>Diener, Per</creator><creator>Ljungdahl, Åke</creator><creator>Khademi, Mohsen</creator><creator>Nilsson, Carl-Gustaf</creator><creator>Olsson, Tomas</creator><general>Elsevier B.V</general><general>Elsevier Science</general><scope>IQODW</scope><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>7TK</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>19960501</creationdate><title>Memantine abrogates neurological deficits, but not CNS inflammation, in Lewis rat experimental autoimmune encephalomyelitis</title><author>Wallström, Erik ; Diener, Per ; Ljungdahl, Åke ; Khademi, Mohsen ; Nilsson, Carl-Gustaf ; Olsson, Tomas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-b7e3a1b093ca9bcfdc89f1daaec230265ae36c58dc2bc72f9a4826fec6963eda3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Animals</topic><topic>Anticonvulsants. Antiepileptics. Antiparkinson agents</topic><topic>Biological and medical sciences</topic><topic>Cell Division - drug effects</topic><topic>Central Nervous System Diseases - drug therapy</topic><topic>Dose-Response Relationship, Drug</topic><topic>Encephalomyelitis, Autoimmune, Experimental - drug therapy</topic><topic>Excitatory Amino Acid Antagonists - therapeutic use</topic><topic>Experimental autoimmune encephalomyelitis (EAE)</topic><topic>Immunohistochemistry</topic><topic>Interferon gamma (IFNγ)</topic><topic>Interferon-gamma - biosynthesis</topic><topic>Interferon-gamma - metabolism</topic><topic>Interferon-gamma - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicin och hälsovetenskap</topic><topic>Memantine</topic><topic>Memantine - therapeutic use</topic><topic>Myelin basic protein (MBP)</topic><topic>Myelin Basic Protein - metabolism</topic><topic>N-methyl- d-aspartate (NMDA) receptor</topic><topic>Neurological deficit</topic><topic>Neuropharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><topic>Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors</topic><topic>RNA, Messenger - analysis</topic><topic>Spinal Cord - chemistry</topic><topic>T-Lymphocytes - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wallström, Erik</creatorcontrib><creatorcontrib>Diener, Per</creatorcontrib><creatorcontrib>Ljungdahl, Åke</creatorcontrib><creatorcontrib>Khademi, Mohsen</creatorcontrib><creatorcontrib>Nilsson, Carl-Gustaf</creatorcontrib><creatorcontrib>Olsson, Tomas</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>SwePub</collection><collection>SwePub Articles</collection><jtitle>Journal of the neurological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wallström, Erik</au><au>Diener, Per</au><au>Ljungdahl, Åke</au><au>Khademi, Mohsen</au><au>Nilsson, Carl-Gustaf</au><au>Olsson, Tomas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Memantine abrogates neurological deficits, but not CNS inflammation, in Lewis rat experimental autoimmune encephalomyelitis</atitle><jtitle>Journal of the neurological sciences</jtitle><addtitle>J Neurol Sci</addtitle><date>1996-05-01</date><risdate>1996</risdate><volume>137</volume><issue>2</issue><spage>89</spage><epage>96</epage><pages>89-96</pages><issn>0022-510X</issn><eissn>1878-5883</eissn><coden>JNSCAG</coden><abstract>Memantine, a clinically employed drug with
N-methyl-
d-aspartate (NMDA) receptor antagonistic effects, dose-dependently ameliorates neurological deficits in Lewis rat experimental autoimmune encephalomyelitis (EAE). Interestingly, this therapeutic effect was not due to dampened CNS inflammation, as assessed by immunohistochemical evaluation of spinal cord tissue. Furthermore, numbers of interferon gamma (IFNγ) mRNA expressing cells were not decreased, as assessed by in situ hybridization. Systemic immunity in terms of numbers of IFNγ secreting cells in response to immunodominant myelin basic protein (MBP) peptides ex vivo was not reduced, and non-toxic doses of memantine did not affect lymphocyte proliferation or IFNγ secretion in vitro. Considering these findings, we hypothesize that effector mechanisms responsible for reversible neurological deficits in EAE may involve NMDA receptors, and this highlights neurons as targets during autoimmune neuroinflammation.</abstract><cop>Shannon</cop><pub>Elsevier B.V</pub><pmid>8782160</pmid><doi>10.1016/0022-510X(95)00339-4</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0022-510X |
| ispartof | Journal of the neurological sciences, 1996-05, Vol.137 (2), p.89-96 |
| issn | 0022-510X 1878-5883 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Animals Anticonvulsants. Antiepileptics. Antiparkinson agents Biological and medical sciences Cell Division - drug effects Central Nervous System Diseases - drug therapy Dose-Response Relationship, Drug Encephalomyelitis, Autoimmune, Experimental - drug therapy Excitatory Amino Acid Antagonists - therapeutic use Experimental autoimmune encephalomyelitis (EAE) Immunohistochemistry Interferon gamma (IFNγ) Interferon-gamma - biosynthesis Interferon-gamma - metabolism Interferon-gamma - physiology Male Medical sciences Medicin och hälsovetenskap Memantine Memantine - therapeutic use Myelin basic protein (MBP) Myelin Basic Protein - metabolism N-methyl- d-aspartate (NMDA) receptor Neurological deficit Neuropharmacology Pharmacology. Drug treatments Rats Rats, Inbred Lew Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors RNA, Messenger - analysis Spinal Cord - chemistry T-Lymphocytes - immunology |
| title | Memantine abrogates neurological deficits, but not CNS inflammation, in Lewis rat experimental autoimmune encephalomyelitis |
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