Dopamine metabolism and neurotransmission in primate brain in relationship to monoamine oxidase A and B inhibition
Identifieur interne : 001F93 ( Main/Corpus ); précédent : 001F92; suivant : 001F94Dopamine metabolism and neurotransmission in primate brain in relationship to monoamine oxidase A and B inhibition
Auteurs : H. Youdim ; P. RiedererSource :
- Journal of Neural Transmission / General Section JNT [ 0300-9564 ] ; 1993-06-01.
Abstract
Summary: The “cheese effect”, potentiation of sympathomimetic action of indirectly acting amines such as tyramine, the main side effect of irreversible nonselective and selective monoamine oxidase (MAO) A inhibitors, has largely been eliminated in the new generation of reversible selective MAO-A and B and irreversible MAO-B inhibitors. These selective inhibitors are demonstrating unique pharmacology and initial controlled clinical studies are providing evidence to support their action as anti-depressants and anti-Parkinson's disease drugs and possibly as neuroprotectors. Thirty years of experience with nonselective MAO inhibitors has resulted in a better understanding and management of the new generation of MAO inhibitors. Because of their selective action on the specific forms of MAO, which results in selective elevation of brain noradrenaline and serotonin on the one hand and dopamine and phenylethylamine on the other, it is hoped that these drugs will be able to elucidate the functional roles of MAO-A and B subtypes with regards to dopamine metabolism in the human brain.
Url:
DOI: 10.1007/BF01245231
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Dopamine metabolism and neurotransmission in primate brain in relationship to monoamine oxidase A and B inhibition</title><author><name sortKey="Youdim, H" sort="Youdim, H" uniqKey="Youdim H" first="H." last="Youdim">H. Youdim</name><affiliation><mods:affiliation>Department of Pharmacology, Technion-Bruce Rappaport Faculty of Medicine, Haifa, Israel</mods:affiliation></affiliation></author><author><name sortKey="Riederer, P" sort="Riederer, P" uniqKey="Riederer P" first="P." last="Riederer">P. Riederer</name><affiliation><mods:affiliation>Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:8BEDF6F24D7CBCC3A995F655D32AB52A022BF610</idno><date when="1993" year="1993">1993</date><idno type="doi">10.1007/BF01245231</idno><idno type="url">https://api.istex.fr/document/8BEDF6F24D7CBCC3A995F655D32AB52A022BF610/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001F93</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Dopamine metabolism and neurotransmission in primate brain in relationship to monoamine oxidase A and B inhibition</title><author><name sortKey="Youdim, H" sort="Youdim, H" uniqKey="Youdim H" first="H." last="Youdim">H. Youdim</name><affiliation><mods:affiliation>Department of Pharmacology, Technion-Bruce Rappaport Faculty of Medicine, Haifa, Israel</mods:affiliation></affiliation></author><author><name sortKey="Riederer, P" sort="Riederer, P" uniqKey="Riederer P" first="P." last="Riederer">P. Riederer</name><affiliation><mods:affiliation>Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neural Transmission / General Section JNT</title><title level="j" type="abbrev">J. Neural Transmission</title><idno type="ISSN">0300-9564</idno><idno type="eISSN">1435-1463</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1993-06-01">1993-06-01</date><biblScope unit="volume">91</biblScope><biblScope unit="issue">2-3</biblScope><biblScope unit="page" from="181">181</biblScope><biblScope unit="page" to="195">195</biblScope></imprint><idno type="ISSN">0300-9564</idno></series><idno type="istex">8BEDF6F24D7CBCC3A995F655D32AB52A022BF610</idno><idno type="DOI">10.1007/BF01245231</idno><idno type="ArticleID">Art5</idno><idno type="ArticleID">BF01245231</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0300-9564</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: The “cheese effect”, potentiation of sympathomimetic action of indirectly acting amines such as tyramine, the main side effect of irreversible nonselective and selective monoamine oxidase (MAO) A inhibitors, has largely been eliminated in the new generation of reversible selective MAO-A and B and irreversible MAO-B inhibitors. These selective inhibitors are demonstrating unique pharmacology and initial controlled clinical studies are providing evidence to support their action as anti-depressants and anti-Parkinson's disease drugs and possibly as neuroprotectors. Thirty years of experience with nonselective MAO inhibitors has resulted in a better understanding and management of the new generation of MAO inhibitors. Because of their selective action on the specific forms of MAO, which results in selective elevation of brain noradrenaline and serotonin on the one hand and dopamine and phenylethylamine on the other, it is hoped that these drugs will be able to elucidate the functional roles of MAO-A and B subtypes with regards to dopamine metabolism in the human brain.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>M. B. H. Youdim</name><affiliations><json:string>Department of Pharmacology, Technion-Bruce Rappaport Faculty of Medicine, Haifa, Israel</json:string></affiliations></json:item><json:item><name>P. Riederer</name><affiliations><json:string>Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</json:string></affiliations></json:item></author><articleId><json:string>Art5</json:string><json:string>BF01245231</json:string></articleId><language><json:string>eng</json:string></language><abstract>Summary: The “cheese effect”, potentiation of sympathomimetic action of indirectly acting amines such as tyramine, the main side effect of irreversible nonselective and selective monoamine oxidase (MAO) A inhibitors, has largely been eliminated in the new generation of reversible selective MAO-A and B and irreversible MAO-B inhibitors. These selective inhibitors are demonstrating unique pharmacology and initial controlled clinical studies are providing evidence to support their action as anti-depressants and anti-Parkinson's disease drugs and possibly as neuroprotectors. Thirty years of experience with nonselective MAO inhibitors has resulted in a better understanding and management of the new generation of MAO inhibitors. Because of their selective action on the specific forms of MAO, which results in selective elevation of brain noradrenaline and serotonin on the one hand and dopamine and phenylethylamine on the other, it is hoped that these drugs will be able to elucidate the functional roles of MAO-A and B subtypes with regards to dopamine metabolism in the human brain.</abstract><qualityIndicators><score>6.908</score><pdfVersion>1.3</pdfVersion><pdfPageSize>576 x 774 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1090</abstractCharCount><pdfWordCount>5385</pdfWordCount><pdfCharCount>33979</pdfCharCount><pdfPageCount>15</pdfPageCount><abstractWordCount>159</abstractWordCount></qualityIndicators><title>Dopamine metabolism and neurotransmission in primate brain in relationship to monoamine oxidase A and B inhibition</title><genre><json:string>research-article</json:string></genre><host><volume>91</volume><pages><last>195</last><first>181</first></pages><issn><json:string>0300-9564</json:string></issn><issue>2-3</issue><subject><json:item><value>Pharmacology/Toxicology</value></json:item><json:item><value>Neurology</value></json:item><json:item><value>Psychiatry</value></json:item></subject><journalId><json:string>702</json:string></journalId><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1435-1463</json:string></eissn><title>Journal of Neural Transmission / General Section JNT</title><publicationDate>1993</publicationDate><copyrightDate>1993</copyrightDate></host><publicationDate>1993</publicationDate><copyrightDate>1993</copyrightDate><doi><json:string>10.1007/BF01245231</json:string></doi><id>8BEDF6F24D7CBCC3A995F655D32AB52A022BF610</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/8BEDF6F24D7CBCC3A995F655D32AB52A022BF610/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/8BEDF6F24D7CBCC3A995F655D32AB52A022BF610/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/8BEDF6F24D7CBCC3A995F655D32AB52A022BF610/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Dopamine metabolism and neurotransmission in primate brain in relationship to monoamine oxidase A and B inhibition</title><respStmt xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><availability><p>SPRINGER</p></availability><date>1992-04-13</date></publicationStmt><notesStmt><note>Full Papers</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Dopamine metabolism and neurotransmission in primate brain in relationship to monoamine oxidase A and B inhibition</title><author><persName><forename type="first">M.</forename><surname>Youdim</surname></persName><affiliation>Department of Pharmacology, Technion-Bruce Rappaport Faculty of Medicine, Haifa, Israel</affiliation></author><author><persName><forename type="first">P.</forename><surname>Riederer</surname></persName><affiliation>Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</affiliation></author></analytic><monogr><title level="j">Journal of Neural Transmission / General Section JNT</title><title level="j" type="abbrev">J. Neural Transmission</title><idno type="JournalID">702</idno><idno type="pISSN">0300-9564</idno><idno type="eISSN">1435-1463</idno><idno type="IssueArticleCount">10</idno><idno type="VolumeIssueCount">3</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1993-06-01"></date><biblScope unit="volume">91</biblScope><biblScope unit="issue">2-3</biblScope><biblScope unit="page" from="181">181</biblScope><biblScope unit="page" to="195">195</biblScope></imprint></monogr><idno type="istex">8BEDF6F24D7CBCC3A995F655D32AB52A022BF610</idno><idno type="DOI">10.1007/BF01245231</idno><idno type="ArticleID">Art5</idno><idno type="ArticleID">BF01245231</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1992-04-13</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Summary: The “cheese effect”, potentiation of sympathomimetic action of indirectly acting amines such as tyramine, the main side effect of irreversible nonselective and selective monoamine oxidase (MAO) A inhibitors, has largely been eliminated in the new generation of reversible selective MAO-A and B and irreversible MAO-B inhibitors. These selective inhibitors are demonstrating unique pharmacology and initial controlled clinical studies are providing evidence to support their action as anti-depressants and anti-Parkinson's disease drugs and possibly as neuroprotectors. Thirty years of experience with nonselective MAO inhibitors has resulted in a better understanding and management of the new generation of MAO inhibitors. Because of their selective action on the specific forms of MAO, which results in selective elevation of brain noradrenaline and serotonin on the one hand and dopamine and phenylethylamine on the other, it is hoped that these drugs will be able to elucidate the functional roles of MAO-A and B subtypes with regards to dopamine metabolism in the human brain.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Pharmacology/Toxicology</term></item><item><term>Neurology</term></item><item><term>Psychiatry</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1992-04-13">Created</change><change when="1993-06-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-2">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/8BEDF6F24D7CBCC3A995F655D32AB52A022BF610/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Springer, Publisher found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer-Verlag</PublisherName><PublisherLocation>Vienna</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>702</JournalID><JournalPrintISSN>0300-9564</JournalPrintISSN><JournalElectronicISSN>1435-1463</JournalElectronicISSN><JournalTitle>Journal of Neural Transmission / General Section JNT</JournalTitle><JournalAbbreviatedTitle>J. 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These selective inhibitors are demonstrating unique pharmacology and initial controlled clinical studies are providing evidence to support their action as anti-depressants and anti-Parkinson's disease drugs and possibly as neuroprotectors. Thirty years of experience with nonselective MAO inhibitors has resulted in a better understanding and management of the new generation of MAO inhibitors. Because of their selective action on the specific forms of MAO, which results in selective elevation of brain noradrenaline and serotonin on the one hand and dopamine and phenylethylamine on the other, it is hoped that these drugs will be able to elucidate the functional roles of MAO-A and B subtypes with regards to dopamine metabolism in the human brain.</Para></Abstract><KeywordGroup Language="En"><Heading>Keywords</Heading><Keyword>Selective irreversible MAO-A and MAO-B inhibitors</Keyword><Keyword>reversible MAO-A inhibitors</Keyword><Keyword>noradrenaline</Keyword><Keyword>dopamine</Keyword><Keyword>serotonin</Keyword><Keyword>depressive illness</Keyword><Keyword>dementia and Parkinson's disease</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Dopamine metabolism and neurotransmission in primate brain in relationship to monoamine oxidase A and B inhibition</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Dopamine metabolism and neurotransmission in primate brain in relationship to monoamine oxidase A and B inhibition</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="given">B.</namePart><namePart type="given">H.</namePart><namePart type="family">Youdim</namePart><affiliation>Department of Pharmacology, Technion-Bruce Rappaport Faculty of Medicine, Haifa, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Riederer</namePart><affiliation>Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Vienna</placeTerm></place><dateCreated encoding="w3cdtf">1992-04-13</dateCreated><dateIssued encoding="w3cdtf">1993-06-01</dateIssued><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Summary: The “cheese effect”, potentiation of sympathomimetic action of indirectly acting amines such as tyramine, the main side effect of irreversible nonselective and selective monoamine oxidase (MAO) A inhibitors, has largely been eliminated in the new generation of reversible selective MAO-A and B and irreversible MAO-B inhibitors. These selective inhibitors are demonstrating unique pharmacology and initial controlled clinical studies are providing evidence to support their action as anti-depressants and anti-Parkinson's disease drugs and possibly as neuroprotectors. Thirty years of experience with nonselective MAO inhibitors has resulted in a better understanding and management of the new generation of MAO inhibitors. Because of their selective action on the specific forms of MAO, which results in selective elevation of brain noradrenaline and serotonin on the one hand and dopamine and phenylethylamine on the other, it is hoped that these drugs will be able to elucidate the functional roles of MAO-A and B subtypes with regards to dopamine metabolism in the human brain.</abstract><note>Full Papers</note><relatedItem type="host"><titleInfo><title>Journal of Neural Transmission / General Section JNT</title></titleInfo><titleInfo type="abbreviated"><title>J. Neural Transmission</title></titleInfo><genre type="Journal" displayLabel="Archive Journal"></genre><originInfo><dateIssued encoding="w3cdtf">1993-06-01</dateIssued><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><subject><genre>Medicine & Public Health</genre><topic>Pharmacology/Toxicology</topic><topic>Neurology</topic><topic>Psychiatry</topic></subject><identifier type="ISSN">0300-9564</identifier><identifier type="eISSN">1435-1463</identifier><identifier type="JournalID">702</identifier><identifier type="IssueArticleCount">10</identifier><identifier type="VolumeIssueCount">3</identifier><part><date>1993</date><detail type="volume"><number>91</number><caption>vol.</caption></detail><detail type="issue"><number>2-3</number><caption>no.</caption></detail><extent unit="pages"><start>181</start><end>195</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 1993</recordOrigin></recordInfo></relatedItem><identifier type="istex">8BEDF6F24D7CBCC3A995F655D32AB52A022BF610</identifier><identifier type="DOI">10.1007/BF01245231</identifier><identifier type="ArticleID">Art5</identifier><identifier type="ArticleID">BF01245231</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag</accessCondition><recordInfo><recordContentSource>SPRINGER</recordContentSource><recordOrigin>Springer-Verlag, 1993</recordOrigin></recordInfo></mods></metadata><enrichments><istex:refBibTEI uri="https://api.istex.fr/document/8BEDF6F24D7CBCC3A995F655D32AB52A022BF610/enrichments/refBib"><teiHeader></teiHeader><text><front></front><body></body><back><listBibl><biblStruct xml:id="b0"><analytic><title level="a" type="main">1990) has provided the evidence for a crucial role of extraneuronal COMT in DA metabolism, which can be an imporant factor in L-dopa efficacy of PD therapy. The inhibition of COMT by these inhibitors The results of these studies suggest (a) inhibition of COMT outside the brain promotes the uptake of L-dopa and (b) inhibition of extraneuronal COMT in the striatum allows sufficient accumulation of DA formed from decarboxylation of L-dopa, which acts postsynaptically to induce the dopamine behavioural syndrome. This effect can be further potentiated by the inhibition of DA uptake with nomifensine (Fig. 7 A, B) The results of these studies have indicated the importance of both extraneuronal MAO-B and COMT in the metabolism and function of DA, formed from L-dopa either intra-or extraneuronally (Fig. 7 A, B) They also point to the extraneuronal metabolism of L-dopa and DA during the L-dopa therapy of Parkinson's disease. Liccione and Azzaro (1988) suggested that the cyclic AMP-induced flux of DA results in a highly significant deamination by MAO- B probably in the glia, but MAO-A was also able to metabolize DA intraneuronally. Indeed, Melamed (1988) has stressed the significance of extraneuronat L-dopa metabolism to the anti-Parkinson action of L-dopa both at the level of decarboxylase and MAO. The compartmentation of MAO-A and -B in the dopaminergic neurons and extraneuronal sites may explain why there are differences in the action of selective MAO-B inhibitors, 1-deprenyl (Riederer and Youdim, 1986) and milacemide (de Varebeke with regards to DA metabolism in primate versus the rodent (rat) brains. They can also clarify why in rat brain selective MAO-A or -B inhibition does not alter brain DA levels or metabolism (Green etal However, in primate brain (human and monkey) 1-deprenyl</title></analytic><monogr><title level="m">The availability of highly active COMT inhibitorsB inhibition followed by L-dopa treatment, induces the behavioural ("dopamine syndrome") action of L-dopa in rats and mice</title><imprint><publisher>DostertRiederer and Youdim</publisher><date type="published" when="1977"></date><biblScope unit="page" from="17" to="19"></biblScope></imprint></monogr><note>and. milacemide (de Varebeke etal, 1990) increase striatal dopamine levels but not as much as that of phenylethylamine. At the present there are no dear indications about References Bevan Jones AB, Pare CMB, etal (1972) Brain amine concentrations after monoamine oxidase inhibitor administration</note></biblStruct><biblStruct xml:id="b1"><analytic><title level="a" type="main">Implications of combined treatment with Madopar and 1-deprenyl in Parkinson's disease</title><author><persName><forename type="first">W</forename><surname>Birkmayer</surname></persName></author><author><persName><forename type="first">P</forename><surname>Riederer</surname></persName></author><author><persName><forename type="first">L</forename><surname>Ambrozi</surname></persName></author></analytic><monogr><title level="j">Lancet</title><imprint><biblScope unit="volume">i</biblScope><biblScope unit="page" from="439" to="444"></biblScope><date type="published" when="1977"></date></imprint></monogr></biblStruct><biblStruct xml:id="b2"><analytic><title level="a" type="main">The potentiation of the antiakinetic effect after L-dopa 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