Sustained release dosage of thyrotropin-releasing hormone improves experimental Japanese encephalitis virus-induced parkinsonism in rats
Identifieur interne : 000271 ( Istex/Corpus ); précédent : 000270; suivant : 000272Sustained release dosage of thyrotropin-releasing hormone improves experimental Japanese encephalitis virus-induced parkinsonism in rats
Auteurs : Akihiko Ogata ; Kazuo Nagashima ; Kotaro Yasui ; Tohru Matsuura ; Kunio TashiroSource :
- Journal of the Neurological Sciences [ 0022-510X ] ; 1998.
English descriptors
- Teeft :
- Adult fischer rats, Basal ganglia, Bilateral substantia nigra, Bradykinesia, Brain striatum, Control rats, Copoly glycolic acid, Dopamine, Dopamine activity, Dopamine levels, Electrochemical detector, Elsevier science, Encephalitis, High performance, Hokkaido university school, Immunohistochemical study, Initial injection, Injection, Japanese encephalitis virus, Monoclonal antibody, Motor activity, Mouse nagoya, Neurochemical alterations, Neurological sciences, Neuropathological changes, Nucleus accumbens, Ogata, Parkinsonian rats, Parkinsonism, Parkinsonism rats, Perchloric acid, Pole test, Possible role, Rat, Release dosage, Release microspheres, Spinocerebellar degeneration, Striatum, Subcutaneous injection, Substantia nigra, Supportive drug, Thyroid function, Times injections.
Abstract
Abstract: Thyrotropin-releasing hormone (TRH) has been reported to have some possibilities toward the treatment of affective CNS disorders. However, long term treatments with daily injections are often required. Effects of TRH-SR (sustained release microspheres of TRH) which is encapsulated in copoly (dl-lactic/glycolic acid) using an in-water drying method were investigated in experimental Japanese encephalitis virus (JEV)-induced post-encephalitic parkinsonism rats by a pole test and high performance liquid chromatography (HPLC) with an electrochemical detector (ECD). We have already reported that in adult Fischer rats killed 12 weeks after infection with JEV at the age of 13 days a marked decrease of tyrosine hydroxylase-positive neurons was found in the bilateral substantia nigra. TRH-SR (3 mg/kg per 2 weeks, 4 times injections, subcutaneous [SC]) improved bradykinesia observed in the JEV-induced parkinsonism rats. Dopamine (DA) concentrations in the JEV-infected rats were profoundly reduced in the striatum as compared with controls. TRH-SR (3 mg/kg, once, SC) increased DA in the striatum 7 days after the injection. Although the pathomechanism of post-encephalitic parkinsonism is different from that of Parkinson's disease and TRH possesses a variety of CNS effects as well, these results suggest that TRH-SR play a possible role in the treatment of Parkinson's disease in addition to post-encephalitic parkinsonism as a supportive drug of l-DOPA.
Url:
DOI: 10.1016/S0022-510X(98)00150-6
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Sustained release dosage of thyrotropin-releasing hormone improves experimental Japanese encephalitis virus-induced parkinsonism in rats</title><author><name sortKey="Ogata, Akihiko" sort="Ogata, Akihiko" uniqKey="Ogata A" first="Akihiko" last="Ogata">Akihiko Ogata</name><affiliation><mods:affiliation>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Corresponding author. Address for correspondence: Department of Neurology, Hokkaido University School of Medicine, North-14, West-5, Kita-ku, Sapporo, 060, Japan. Tel.: +81 11 7161161, ext 6028; fax: +81 11 7005356; e-mail: a-ogata@med.hokudai.ac.jp</mods:affiliation></affiliation></author><author><name sortKey="Nagashima, Kazuo" sort="Nagashima, Kazuo" uniqKey="Nagashima K" first="Kazuo" last="Nagashima">Kazuo Nagashima</name><affiliation><mods:affiliation>Department of Pathology, Hokkaido University School of Medicine, Sapporo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Yasui, Kotaro" sort="Yasui, Kotaro" uniqKey="Yasui K" first="Kotaro" last="Yasui">Kotaro Yasui</name><affiliation><mods:affiliation>Department of Microbiology and Immunology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Matsuura, Tohru" sort="Matsuura, Tohru" uniqKey="Matsuura T" first="Tohru" last="Matsuura">Tohru Matsuura</name><affiliation><mods:affiliation>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Tashiro, Kunio" sort="Tashiro, Kunio" uniqKey="Tashiro K" first="Kunio" last="Tashiro">Kunio Tashiro</name><affiliation><mods:affiliation>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:DFE7CE8F18C308DF87F70FEAACECE86564B3B6CE</idno><date when="1998" year="1998">1998</date><idno type="doi">10.1016/S0022-510X(98)00150-6</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-CGJNR1DF-7/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000271</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000271</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Sustained release dosage of thyrotropin-releasing hormone improves experimental Japanese encephalitis virus-induced parkinsonism in rats</title><author><name sortKey="Ogata, Akihiko" sort="Ogata, Akihiko" uniqKey="Ogata A" first="Akihiko" last="Ogata">Akihiko Ogata</name><affiliation><mods:affiliation>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Corresponding author. Address for correspondence: Department of Neurology, Hokkaido University School of Medicine, North-14, West-5, Kita-ku, Sapporo, 060, Japan. Tel.: +81 11 7161161, ext 6028; fax: +81 11 7005356; e-mail: a-ogata@med.hokudai.ac.jp</mods:affiliation></affiliation></author><author><name sortKey="Nagashima, Kazuo" sort="Nagashima, Kazuo" uniqKey="Nagashima K" first="Kazuo" last="Nagashima">Kazuo Nagashima</name><affiliation><mods:affiliation>Department of Pathology, Hokkaido University School of Medicine, Sapporo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Yasui, Kotaro" sort="Yasui, Kotaro" uniqKey="Yasui K" first="Kotaro" last="Yasui">Kotaro Yasui</name><affiliation><mods:affiliation>Department of Microbiology and Immunology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Matsuura, Tohru" sort="Matsuura, Tohru" uniqKey="Matsuura T" first="Tohru" last="Matsuura">Tohru Matsuura</name><affiliation><mods:affiliation>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Tashiro, Kunio" sort="Tashiro, Kunio" uniqKey="Tashiro K" first="Kunio" last="Tashiro">Kunio Tashiro</name><affiliation><mods:affiliation>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="ISSN">0022-510X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998">1998</date><biblScope unit="volume">159</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="135">135</biblScope><biblScope unit="page" to="139">139</biblScope></imprint><idno type="ISSN">0022-510X</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-510X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Adult fischer rats</term><term>Basal ganglia</term><term>Bilateral substantia nigra</term><term>Bradykinesia</term><term>Brain striatum</term><term>Control rats</term><term>Copoly glycolic acid</term><term>Dopamine</term><term>Dopamine activity</term><term>Dopamine levels</term><term>Electrochemical detector</term><term>Elsevier science</term><term>Encephalitis</term><term>High performance</term><term>Hokkaido university school</term><term>Immunohistochemical study</term><term>Initial injection</term><term>Injection</term><term>Japanese encephalitis virus</term><term>Monoclonal antibody</term><term>Motor activity</term><term>Mouse nagoya</term><term>Neurochemical alterations</term><term>Neurological sciences</term><term>Neuropathological changes</term><term>Nucleus accumbens</term><term>Ogata</term><term>Parkinsonian rats</term><term>Parkinsonism</term><term>Parkinsonism rats</term><term>Perchloric acid</term><term>Pole test</term><term>Possible role</term><term>Rat</term><term>Release dosage</term><term>Release microspheres</term><term>Spinocerebellar degeneration</term><term>Striatum</term><term>Subcutaneous injection</term><term>Substantia nigra</term><term>Supportive drug</term><term>Thyroid function</term><term>Times injections</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Thyrotropin-releasing hormone (TRH) has been reported to have some possibilities toward the treatment of affective CNS disorders. However, long term treatments with daily injections are often required. Effects of TRH-SR (sustained release microspheres of TRH) which is encapsulated in copoly (dl-lactic/glycolic acid) using an in-water drying method were investigated in experimental Japanese encephalitis virus (JEV)-induced post-encephalitic parkinsonism rats by a pole test and high performance liquid chromatography (HPLC) with an electrochemical detector (ECD). We have already reported that in adult Fischer rats killed 12 weeks after infection with JEV at the age of 13 days a marked decrease of tyrosine hydroxylase-positive neurons was found in the bilateral substantia nigra. TRH-SR (3 mg/kg per 2 weeks, 4 times injections, subcutaneous [SC]) improved bradykinesia observed in the JEV-induced parkinsonism rats. Dopamine (DA) concentrations in the JEV-infected rats were profoundly reduced in the striatum as compared with controls. TRH-SR (3 mg/kg, once, SC) increased DA in the striatum 7 days after the injection. Although the pathomechanism of post-encephalitic parkinsonism is different from that of Parkinson's disease and TRH possesses a variety of CNS effects as well, these results suggest that TRH-SR play a possible role in the treatment of Parkinson's disease in addition to post-encephalitic parkinsonism as a supportive drug of l-DOPA.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>parkinsonism</json:string><json:string>dopamine</json:string><json:string>striatum</json:string><json:string>control rats</json:string><json:string>ogata</json:string><json:string>bradykinesia</json:string><json:string>neurological sciences</json:string><json:string>pole test</json:string><json:string>parkinsonism rats</json:string><json:string>encephalitis</json:string><json:string>copoly glycolic acid</json:string><json:string>monoclonal antibody</json:string><json:string>rat</json:string><json:string>mouse nagoya</json:string><json:string>times injections</json:string><json:string>substantia nigra</json:string><json:string>hokkaido university school</json:string><json:string>adult fischer rats</json:string><json:string>bilateral substantia nigra</json:string><json:string>nucleus accumbens</json:string><json:string>possible role</json:string><json:string>release dosage</json:string><json:string>elsevier science</json:string><json:string>japanese encephalitis virus</json:string><json:string>spinocerebellar degeneration</json:string><json:string>neurochemical alterations</json:string><json:string>dopamine activity</json:string><json:string>high performance</json:string><json:string>subcutaneous injection</json:string><json:string>perchloric acid</json:string><json:string>neuropathological changes</json:string><json:string>parkinsonian rats</json:string><json:string>electrochemical detector</json:string><json:string>immunohistochemical study</json:string><json:string>dopamine levels</json:string><json:string>brain striatum</json:string><json:string>motor activity</json:string><json:string>initial injection</json:string><json:string>basal ganglia</json:string><json:string>thyroid function</json:string><json:string>release microspheres</json:string><json:string>supportive drug</json:string><json:string>injection</json:string></teeft></keywords><author><json:item><name>Akihiko Ogata</name><affiliations><json:string>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</json:string><json:string>Corresponding author. Address for correspondence: Department of Neurology, Hokkaido University School of Medicine, North-14, West-5, Kita-ku, Sapporo, 060, Japan. Tel.: +81 11 7161161, ext 6028; fax: +81 11 7005356; e-mail: a-ogata@med.hokudai.ac.jp</json:string></affiliations></json:item><json:item><name>Kazuo Nagashima</name><affiliations><json:string>Department of Pathology, Hokkaido University School of Medicine, Sapporo, Japan</json:string></affiliations></json:item><json:item><name>Kotaro Yasui</name><affiliations><json:string>Department of Microbiology and Immunology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Tohru Matsuura</name><affiliations><json:string>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</json:string></affiliations></json:item><json:item><name>Kunio Tashiro</name><affiliations><json:string>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Japanese encephalitis virus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Post-encephalitic parkinsonism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Thyrotropin-releasing hormone (TRH)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Treatment</value></json:item></subject><arkIstex>ark:/67375/6H6-CGJNR1DF-7</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Thyrotropin-releasing hormone (TRH) has been reported to have some possibilities toward the treatment of affective CNS disorders. However, long term treatments with daily injections are often required. Effects of TRH-SR (sustained release microspheres of TRH) which is encapsulated in copoly (dl-lactic/glycolic acid) using an in-water drying method were investigated in experimental Japanese encephalitis virus (JEV)-induced post-encephalitic parkinsonism rats by a pole test and high performance liquid chromatography (HPLC) with an electrochemical detector (ECD). We have already reported that in adult Fischer rats killed 12 weeks after infection with JEV at the age of 13 days a marked decrease of tyrosine hydroxylase-positive neurons was found in the bilateral substantia nigra. TRH-SR (3 mg/kg per 2 weeks, 4 times injections, subcutaneous [SC]) improved bradykinesia observed in the JEV-induced parkinsonism rats. Dopamine (DA) concentrations in the JEV-infected rats were profoundly reduced in the striatum as compared with controls. TRH-SR (3 mg/kg, once, SC) increased DA in the striatum 7 days after the injection. Although the pathomechanism of post-encephalitic parkinsonism is different from that of Parkinson's disease and TRH possesses a variety of CNS effects as well, these results suggest that TRH-SR play a possible role in the treatment of Parkinson's disease in addition to post-encephalitic parkinsonism as a supportive drug of l-DOPA.</abstract><qualityIndicators><score>7.138</score><pdfWordCount>2618</pdfWordCount><pdfCharCount>17016</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>5</pdfPageCount><pdfPageSize>598 x 798 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>210</abstractWordCount><abstractCharCount>1470</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Sustained release dosage of thyrotropin-releasing hormone improves experimental Japanese encephalitis virus-induced parkinsonism in rats</title><pmid><json:string>9741396</json:string></pmid><pii><json:string>S0022-510X(98)00150-6</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>Journal of the Neurological Sciences</title><language><json:string>unknown</json:string></language><publicationDate>1998</publicationDate><issn><json:string>0022-510X</json:string></issn><pii><json:string>S0022-510X(00)X0060-3</json:string></pii><volume>159</volume><issue>2</issue><pages><first>135</first><last>139</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1998</json:string></date><geogName></geogName><orgName><json:string>Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan</json:string><json:string>Department of Neurology, Hokkaido University School of Medicine, North</json:string><json:string>Department of Microbiology and Immunology</json:string><json:string>Takeda Chemical Industries</json:string><json:string>Research Committee of CNS Degenerative Diseases</json:string><json:string>Japan</json:string><json:string>Ministry of Health and Welfare</json:string></orgName><orgName_funder><json:string>Research Committee of CNS Degenerative Diseases</json:string><json:string>Japan</json:string><json:string>Ministry of Health and Welfare</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Kenichi Nakase</json:string></persName><placeName><json:string>Japan</json:string><json:string>Tokyo</json:string><json:string>Sapporo</json:string><json:string>Osaka</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>[4]</json:string><json:string>[21,22]</json:string><json:string>[23]</json:string><json:string>[18]</json:string><json:string>[6]</json:string><json:string>Nagai et al. [9]</json:string><json:string>[2,3]</json:string><json:string>[8]</json:string><json:string>[17]</json:string><json:string>[1]</json:string><json:string>[21]</json:string><json:string>[16]</json:string><json:string>[3]</json:string><json:string>[13,14]</json:string><json:string>[20]</json:string><json:string>[5]</json:string><json:string>[15]</json:string><json:string>A. Ogata et al.</json:string><json:string>[7]</json:string><json:string>[21,25,26]</json:string><json:string>[2]</json:string><json:string>[24]</json:string><json:string>[19]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-CGJNR1DF-7</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - neurosciences</json:string><json:string>2 - clinical neurology</json:string></wos><scienceMetrix></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Clinical Neurology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Neuroscience</json:string><json:string>3 - Neurology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string><json:string>4 - pathologie infectieuse</json:string></inist></categories><publicationDate>1998</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1016/S0022-510X(98)00150-6</json:string></doi><id>DFE7CE8F18C308DF87F70FEAACECE86564B3B6CE</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-CGJNR1DF-7/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-CGJNR1DF-7/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-CGJNR1DF-7/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">Sustained release dosage of thyrotropin-releasing hormone improves experimental Japanese encephalitis virus-induced parkinsonism in rats</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>©1998 Elsevier Science B.V.</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</p></availability><date>1998</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note type="content">Fig. 1: TRH-SR (3 mg/kg per 2 weeks, 4 times injections, subcutaneous) improves bradykinesia in JEV-induced parkinsonism rats. The difference between the JEV-infected rats and the rats after 4 times TRH-SR injections is significant (P<0.001).</note><note type="content">Fig. 2: Immunohistochemical study of the midbrain with anti-tyrosine hydroxylase (TH) antibody in a JEV-induced parkinsonism rat (a) and an age-matched control rat (b). x20. TH-positive neurons in a JEV-infected rat (a) are decreased in number in the substantia nigra compared with those in a control rat (b).</note><note type="content">Table 1: Dopamine levels of brain striatum in control rats, JEV-infected rats, and JEV-infected rats with TRH-SR injection</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Sustained release dosage of thyrotropin-releasing hormone improves experimental Japanese encephalitis virus-induced parkinsonism in rats</title><author xml:id="author-0000"><persName><forename type="first">Akihiko</forename><surname>Ogata</surname></persName><affiliation>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</affiliation><affiliation>Corresponding author. Address for correspondence: Department of Neurology, Hokkaido University School of Medicine, North-14, West-5, Kita-ku, Sapporo, 060, Japan. Tel.: +81 11 7161161, ext 6028; fax: +81 11 7005356; e-mail: a-ogata@med.hokudai.ac.jp</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Kazuo</forename><surname>Nagashima</surname></persName><affiliation>Department of Pathology, Hokkaido University School of Medicine, Sapporo, Japan</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Kotaro</forename><surname>Yasui</surname></persName><affiliation>Department of Microbiology and Immunology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Tohru</forename><surname>Matsuura</surname></persName><affiliation>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Kunio</forename><surname>Tashiro</surname></persName><affiliation>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</affiliation></author><idno type="istex">DFE7CE8F18C308DF87F70FEAACECE86564B3B6CE</idno><idno type="ark">ark:/67375/6H6-CGJNR1DF-7</idno><idno type="DOI">10.1016/S0022-510X(98)00150-6</idno><idno type="PII">S0022-510X(98)00150-6</idno></analytic><monogr><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="pISSN">0022-510X</idno><idno type="PII">S0022-510X(00)X0060-3</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998"></date><biblScope unit="volume">159</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="135">135</biblScope><biblScope unit="page" to="139">139</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Thyrotropin-releasing hormone (TRH) has been reported to have some possibilities toward the treatment of affective CNS disorders. However, long term treatments with daily injections are often required. Effects of TRH-SR (sustained release microspheres of TRH) which is encapsulated in copoly (dl-lactic/glycolic acid) using an in-water drying method were investigated in experimental Japanese encephalitis virus (JEV)-induced post-encephalitic parkinsonism rats by a pole test and high performance liquid chromatography (HPLC) with an electrochemical detector (ECD). We have already reported that in adult Fischer rats killed 12 weeks after infection with JEV at the age of 13 days a marked decrease of tyrosine hydroxylase-positive neurons was found in the bilateral substantia nigra. TRH-SR (3 mg/kg per 2 weeks, 4 times injections, subcutaneous [SC]) improved bradykinesia observed in the JEV-induced parkinsonism rats. Dopamine (DA) concentrations in the JEV-infected rats were profoundly reduced in the striatum as compared with controls. TRH-SR (3 mg/kg, once, SC) increased DA in the striatum 7 days after the injection. Although the pathomechanism of post-encephalitic parkinsonism is different from that of Parkinson's disease and TRH possesses a variety of CNS effects as well, these results suggest that TRH-SR play a possible role in the treatment of Parkinson's disease in addition to post-encephalitic parkinsonism as a supportive drug of l-DOPA.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Japanese encephalitis virus</term></item><item><term>Post-encephalitic parkinsonism</term></item><item><term>Parkinson's disease</term></item><item><term>Thyrotropin-releasing hormone (TRH)</term></item><item><term>Treatment</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1998-04-16">Modified</change><change when="1998">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-CGJNR1DF-7/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="gr1"></istex:entity><istex:entity SYSTEM="gr2" NDATA="IMAGE" name="gr2"></istex:entity></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>JNS</jid><aid>5813</aid><ce:pii>S0022-510X(98)00150-6</ce:pii><ce:doi>10.1016/S0022-510X(98)00150-6</ce:doi><ce:copyright year="1998" type="full-transfer">Elsevier Science B.V.</ce:copyright></item-info><head><ce:title>Sustained release dosage of thyrotropin-releasing hormone improves experimental Japanese encephalitis virus-induced parkinsonism in rats</ce:title><ce:author-group><ce:author><ce:given-name>Akihiko</ce:given-name><ce:surname>Ogata</ce:surname><ce:cross-ref refid="AFF1">a</ce:cross-ref><ce:cross-ref refid="CORR1">*</ce:cross-ref></ce:author><ce:author><ce:given-name>Kazuo</ce:given-name><ce:surname>Nagashima</ce:surname><ce:cross-ref refid="AFF2">b</ce:cross-ref></ce:author><ce:author><ce:given-name>Kotaro</ce:given-name><ce:surname>Yasui</ce:surname><ce:cross-ref refid="AFF3">c</ce:cross-ref></ce:author><ce:author><ce:given-name>Tohru</ce:given-name><ce:surname>Matsuura</ce:surname><ce:cross-ref refid="AFF1">a</ce:cross-ref></ce:author><ce:author><ce:given-name>Kunio</ce:given-name><ce:surname>Tashiro</ce:surname><ce:cross-ref refid="AFF1">a</ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Pathology, Hokkaido University School of Medicine, Sapporo, Japan</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Department of Microbiology and Immunology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Corresponding author. Address for correspondence: Department of Neurology, Hokkaido University School of Medicine, North-14, West-5, Kita-ku, Sapporo, 060, Japan. Tel.: +81 11 7161161, ext 6028; fax: +81 11 7005356; e-mail: a-ogata@med.hokudai.ac.jp</ce:text></ce:correspondence></ce:author-group><ce:date-received day="26" month="11" year="1997"></ce:date-received><ce:date-revised day="16" month="4" year="1998"></ce:date-revised><ce:date-accepted day="16" month="4" year="1998"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Thyrotropin-releasing hormone (TRH) has been reported to have some possibilities toward the treatment of affective CNS disorders. However, long term treatments with daily injections are often required. Effects of TRH-SR (sustained release microspheres of TRH) which is encapsulated in copoly (dl-lactic/glycolic acid) using an in-water drying method were investigated in experimental Japanese encephalitis virus (JEV)-induced post-encephalitic parkinsonism rats by a pole test and high performance liquid chromatography (HPLC) with an electrochemical detector (ECD). We have already reported that in adult Fischer rats killed 12 weeks after infection with JEV at the age of 13 days a marked decrease of tyrosine hydroxylase-positive neurons was found in the bilateral substantia nigra. TRH-SR (3 mg/kg per 2 weeks, 4 times injections, subcutaneous [SC]) improved bradykinesia observed in the JEV-induced parkinsonism rats. Dopamine (DA) concentrations in the JEV-infected rats were profoundly reduced in the striatum as compared with controls. TRH-SR (3 mg/kg, once, SC) increased DA in the striatum 7 days after the injection. Although the pathomechanism of post-encephalitic parkinsonism is different from that of Parkinson's disease and TRH possesses a variety of CNS effects as well, these results suggest that TRH-SR play a possible role in the treatment of Parkinson's disease in addition to post-encephalitic parkinsonism as a supportive drug of <ce:small-caps>l</ce:small-caps>-DOPA.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Japanese encephalitis virus</ce:text></ce:keyword><ce:keyword><ce:text>Post-encephalitic parkinsonism</ce:text></ce:keyword><ce:keyword><ce:text>Parkinson's disease</ce:text></ce:keyword><ce:keyword><ce:text>Thyrotropin-releasing hormone (TRH)</ce:text></ce:keyword><ce:keyword><ce:text>Treatment</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Sustained release dosage of thyrotropin-releasing hormone improves experimental Japanese encephalitis virus-induced parkinsonism in rats</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Sustained release dosage of thyrotropin-releasing hormone improves experimental Japanese encephalitis virus-induced parkinsonism in rats</title></titleInfo><name type="personal"><namePart type="given">Akihiko</namePart><namePart type="family">Ogata</namePart><affiliation>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</affiliation><affiliation>Corresponding author. Address for correspondence: Department of Neurology, Hokkaido University School of Medicine, North-14, West-5, Kita-ku, Sapporo, 060, Japan. Tel.: +81 11 7161161, ext 6028; fax: +81 11 7005356; e-mail: a-ogata@med.hokudai.ac.jp</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kazuo</namePart><namePart type="family">Nagashima</namePart><affiliation>Department of Pathology, Hokkaido University School of Medicine, Sapporo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kotaro</namePart><namePart type="family">Yasui</namePart><affiliation>Department of Microbiology and Immunology, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tohru</namePart><namePart type="family">Matsuura</namePart><affiliation>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kunio</namePart><namePart type="family">Tashiro</namePart><affiliation>Department of Neurology, Hokkaido University School of Medicine, Sapporo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1998</dateIssued><dateModified encoding="w3cdtf">1998-04-16</dateModified><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Thyrotropin-releasing hormone (TRH) has been reported to have some possibilities toward the treatment of affective CNS disorders. However, long term treatments with daily injections are often required. Effects of TRH-SR (sustained release microspheres of TRH) which is encapsulated in copoly (dl-lactic/glycolic acid) using an in-water drying method were investigated in experimental Japanese encephalitis virus (JEV)-induced post-encephalitic parkinsonism rats by a pole test and high performance liquid chromatography (HPLC) with an electrochemical detector (ECD). We have already reported that in adult Fischer rats killed 12 weeks after infection with JEV at the age of 13 days a marked decrease of tyrosine hydroxylase-positive neurons was found in the bilateral substantia nigra. TRH-SR (3 mg/kg per 2 weeks, 4 times injections, subcutaneous [SC]) improved bradykinesia observed in the JEV-induced parkinsonism rats. Dopamine (DA) concentrations in the JEV-infected rats were profoundly reduced in the striatum as compared with controls. TRH-SR (3 mg/kg, once, SC) increased DA in the striatum 7 days after the injection. Although the pathomechanism of post-encephalitic parkinsonism is different from that of Parkinson's disease and TRH possesses a variety of CNS effects as well, these results suggest that TRH-SR play a possible role in the treatment of Parkinson's disease in addition to post-encephalitic parkinsonism as a supportive drug of l-DOPA.</abstract><note type="content">Fig. 1: TRH-SR (3 mg/kg per 2 weeks, 4 times injections, subcutaneous) improves bradykinesia in JEV-induced parkinsonism rats. The difference between the JEV-infected rats and the rats after 4 times TRH-SR injections is significant (P<0.001).</note><note type="content">Fig. 2: Immunohistochemical study of the midbrain with anti-tyrosine hydroxylase (TH) antibody in a JEV-induced parkinsonism rat (a) and an age-matched control rat (b). x20. TH-positive neurons in a JEV-infected rat (a) are decreased in number in the substantia nigra compared with those in a control rat (b).</note><note type="content">Table 1: Dopamine levels of brain striatum in control rats, JEV-infected rats, and JEV-infected rats with TRH-SR injection</note><subject><genre>Keywords</genre><topic>Japanese encephalitis virus</topic><topic>Post-encephalitic parkinsonism</topic><topic>Parkinson's disease</topic><topic>Thyrotropin-releasing hormone (TRH)</topic><topic>Treatment</topic></subject><relatedItem type="host"><titleInfo><title>Journal of the Neurological Sciences</title></titleInfo><titleInfo type="abbreviated"><title>JNS</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1998</dateIssued></originInfo><identifier type="ISSN">0022-510X</identifier><identifier type="PII">S0022-510X(00)X0060-3</identifier><part><date>1998</date><detail type="volume"><number>159</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue-pages"><start>121</start><end>244</end></extent><extent unit="pages"><start>135</start><end>139</end></extent></part></relatedItem><identifier type="istex">DFE7CE8F18C308DF87F70FEAACECE86564B3B6CE</identifier><identifier type="ark">ark:/67375/6H6-CGJNR1DF-7</identifier><identifier type="DOI">10.1016/S0022-510X(98)00150-6</identifier><identifier type="PII">S0022-510X(98)00150-6</identifier><accessCondition type="use and reproduction" contentType="copyright">©1998 Elsevier Science B.V.</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>Elsevier Science B.V., ©1998</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-CGJNR1DF-7/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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