In vitro studies on the possible effects of 1-aminoadamantanes on the serotonergic system in M. Parkinson
Identifieur interne : 000687 ( Main/Corpus ); précédent : 000686; suivant : 000688In vitro studies on the possible effects of 1-aminoadamantanes on the serotonergic system in M. Parkinson
Auteurs : W. Wesemann ; G. Dette-Wildenhahn ; H. FellehnerSource :
- Journal of Neural Transmission [ 0300-9564 ] ; 1979-12-01.
Abstract
Summary: Synaptosomes, synaptic vesicles, and membranes were isolated from rat brain homogenates by differential and density gradient centrifugation in sucrose. Synaptosomes incorporated serotonin (5-HT) with two different uptake mechanisms, high affinity: Kt1=47 nM and low affinity: Kt2=660 nM. Both uptake mechanisms are non-competitively inhibited by the potential antiparkinson drugs 1-aminoadamantane (amantadine, D 1: Ki1=57μM, Ki2=96μM) and 1-amino-3.5-dimethyladamantane (memantine, D 145: Ki1=97μM, Ki2=150μM). The incorporated 5-HT is released from Synaptosomes on incubation with high concentrations (0.5–5 mM) of the drugs or on electrical stimulation with rectangular pulses of alternating polarity. Subthreshold concentrations of these drugs (5–50μM) which are too low to liberate 5-HT increase the electrically stimulated release of 5-HT.—The effect of D 1, D 145, and electrical stimulation on DA release parallels the results observed with 5-HT. The uptake of 5-HT into isolated synaptic vesicles and the binding to isolated nerve ending membranes is non-competitively inhibited by 1-aminoadamantanes. D 145 inhibits the binding of 5-HT to membranes more effectively (Ki=0.95 mM) than its uptake into vesicles (Ki=1.2mM) contrasting with D 1 which is a weaker inhibitor affecting vesicular uptake (Ki=2.5 mM) slightly more than membrane binding (Ki=3.1 mM). The results obtained suggest that, in addition to other mechanisms like receptor stimulation, 1-aminoadamantanes may act in parkinsonian patients by enriching the transmitter content in the synaptic cleft.
Url:
DOI: 10.1007/BF01250322
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Dette-Wildenhahn</name><affiliation><mods:affiliation>Abteilung für Neurodiemie, Physiologisch-chemisches Institut II, Philipps-Universität, Marburg/Lahn, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Fellehner, H" sort="Fellehner, H" uniqKey="Fellehner H" first="H." last="Fellehner">H. 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Wesemann</name><affiliation><mods:affiliation>Abteilung für Neurodiemie, Physiologisch-chemisches Institut II, Philipps-Universität, Marburg/Lahn, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Dette Wildenhahn, G" sort="Dette Wildenhahn, G" uniqKey="Dette Wildenhahn G" first="G." last="Dette-Wildenhahn">G. Dette-Wildenhahn</name><affiliation><mods:affiliation>Abteilung für Neurodiemie, Physiologisch-chemisches Institut II, Philipps-Universität, Marburg/Lahn, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Fellehner, H" sort="Fellehner, H" uniqKey="Fellehner H" first="H." last="Fellehner">H. 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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="1979-12-01">1979-12-01</date><biblScope unit="volume">44</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="263">263</biblScope><biblScope unit="page" to="285">285</biblScope></imprint><idno type="ISSN">0300-9564</idno></series><idno type="istex">5CB6105AED86AF7058C521EEA6FC481340D26CD4</idno><idno type="DOI">10.1007/BF01250322</idno><idno type="ArticleID">Art2</idno><idno type="ArticleID">BF01250322</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: Synaptosomes, synaptic vesicles, and membranes were isolated from rat brain homogenates by differential and density gradient centrifugation in sucrose. Synaptosomes incorporated serotonin (5-HT) with two different uptake mechanisms, high affinity: Kt1=47 nM and low affinity: Kt2=660 nM. Both uptake mechanisms are non-competitively inhibited by the potential antiparkinson drugs 1-aminoadamantane (amantadine, D 1: Ki1=57μM, Ki2=96μM) and 1-amino-3.5-dimethyladamantane (memantine, D 145: Ki1=97μM, Ki2=150μM). The incorporated 5-HT is released from Synaptosomes on incubation with high concentrations (0.5–5 mM) of the drugs or on electrical stimulation with rectangular pulses of alternating polarity. Subthreshold concentrations of these drugs (5–50μM) which are too low to liberate 5-HT increase the electrically stimulated release of 5-HT.—The effect of D 1, D 145, and electrical stimulation on DA release parallels the results observed with 5-HT. The uptake of 5-HT into isolated synaptic vesicles and the binding to isolated nerve ending membranes is non-competitively inhibited by 1-aminoadamantanes. D 145 inhibits the binding of 5-HT to membranes more effectively (Ki=0.95 mM) than its uptake into vesicles (Ki=1.2mM) contrasting with D 1 which is a weaker inhibitor affecting vesicular uptake (Ki=2.5 mM) slightly more than membrane binding (Ki=3.1 mM). The results obtained suggest that, in addition to other mechanisms like receptor stimulation, 1-aminoadamantanes may act in parkinsonian patients by enriching the transmitter content in the synaptic cleft.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>W. Wesemann</name><affiliations><json:string>Abteilung für Neurodiemie, Physiologisch-chemisches Institut II, Philipps-Universität, Marburg/Lahn, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>G. Dette-Wildenhahn</name><affiliations><json:string>Abteilung für Neurodiemie, Physiologisch-chemisches Institut II, Philipps-Universität, Marburg/Lahn, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>H. Fellehner</name><affiliations><json:string>Abteilung für Neurodiemie, Physiologisch-chemisches Institut II, Philipps-Universität, Marburg/Lahn, Federal Republic of Germany</json:string></affiliations></json:item></author><articleId><json:string>Art2</json:string><json:string>BF01250322</json:string></articleId><language><json:string>eng</json:string></language><abstract>Summary: Synaptosomes, synaptic vesicles, and membranes were isolated from rat brain homogenates by differential and density gradient centrifugation in sucrose. Synaptosomes incorporated serotonin (5-HT) with two different uptake mechanisms, high affinity: Kt1=47 nM and low affinity: Kt2=660 nM. Both uptake mechanisms are non-competitively inhibited by the potential antiparkinson drugs 1-aminoadamantane (amantadine, D 1: Ki1=57μM, Ki2=96μM) and 1-amino-3.5-dimethyladamantane (memantine, D 145: Ki1=97μM, Ki2=150μM). The incorporated 5-HT is released from Synaptosomes on incubation with high concentrations (0.5–5 mM) of the drugs or on electrical stimulation with rectangular pulses of alternating polarity. Subthreshold concentrations of these drugs (5–50μM) which are too low to liberate 5-HT increase the electrically stimulated release of 5-HT.—The effect of D 1, D 145, and electrical stimulation on DA release parallels the results observed with 5-HT. The uptake of 5-HT into isolated synaptic vesicles and the binding to isolated nerve ending membranes is non-competitively inhibited by 1-aminoadamantanes. D 145 inhibits the binding of 5-HT to membranes more effectively (Ki=0.95 mM) than its uptake into vesicles (Ki=1.2mM) contrasting with D 1 which is a weaker inhibitor affecting vesicular uptake (Ki=2.5 mM) slightly more than membrane binding (Ki=3.1 mM). The results obtained suggest that, in addition to other mechanisms like receptor stimulation, 1-aminoadamantanes may act in parkinsonian patients by enriching the transmitter content in the synaptic cleft.</abstract><qualityIndicators><score>7.592</score><pdfVersion>1.3</pdfVersion><pdfPageSize>432 x 648 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1581</abstractCharCount><pdfWordCount>7405</pdfWordCount><pdfCharCount>43050</pdfCharCount><pdfPageCount>23</pdfPageCount><abstractWordCount>216</abstractWordCount></qualityIndicators><title>In vitro studies on the possible effects of 1-aminoadamantanes on the serotonergic system in M. 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Parkinson</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>1978-09-11</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">In vitro studies on the possible effects of 1-aminoadamantanes on the serotonergic system in M. Parkinson</title><author><persName><forename type="first">W.</forename><surname>Wesemann</surname></persName><affiliation>Abteilung für Neurodiemie, Physiologisch-chemisches Institut II, Philipps-Universität, Marburg/Lahn, Federal Republic of Germany</affiliation></author><author><persName><forename type="first">G.</forename><surname>Dette-Wildenhahn</surname></persName><affiliation>Abteilung für Neurodiemie, Physiologisch-chemisches Institut II, Philipps-Universität, Marburg/Lahn, Federal Republic of Germany</affiliation></author><author><persName><forename type="first">H.</forename><surname>Fellehner</surname></persName><affiliation>Abteilung für Neurodiemie, Physiologisch-chemisches Institut II, Philipps-Universität, Marburg/Lahn, Federal Republic of Germany</affiliation></author></analytic><monogr><title level="j">Journal of Neural Transmission</title><title level="j" type="sub">Basic neurosciences and genetics, Parkinson's disease and allied conditions, Alzheimer's disease and related disorders, biological psychiatry</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">4</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1979-12-01"></date><biblScope unit="volume">44</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="263">263</biblScope><biblScope unit="page" to="285">285</biblScope></imprint></monogr><idno type="istex">5CB6105AED86AF7058C521EEA6FC481340D26CD4</idno><idno type="DOI">10.1007/BF01250322</idno><idno type="ArticleID">Art2</idno><idno type="ArticleID">BF01250322</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1978-09-11</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Summary: Synaptosomes, synaptic vesicles, and membranes were isolated from rat brain homogenates by differential and density gradient centrifugation in sucrose. Synaptosomes incorporated serotonin (5-HT) with two different uptake mechanisms, high affinity: Kt1=47 nM and low affinity: Kt2=660 nM. Both uptake mechanisms are non-competitively inhibited by the potential antiparkinson drugs 1-aminoadamantane (amantadine, D 1: Ki1=57μM, Ki2=96μM) and 1-amino-3.5-dimethyladamantane (memantine, D 145: Ki1=97μM, Ki2=150μM). The incorporated 5-HT is released from Synaptosomes on incubation with high concentrations (0.5–5 mM) of the drugs or on electrical stimulation with rectangular pulses of alternating polarity. Subthreshold concentrations of these drugs (5–50μM) which are too low to liberate 5-HT increase the electrically stimulated release of 5-HT.—The effect of D 1, D 145, and electrical stimulation on DA release parallels the results observed with 5-HT. The uptake of 5-HT into isolated synaptic vesicles and the binding to isolated nerve ending membranes is non-competitively inhibited by 1-aminoadamantanes. D 145 inhibits the binding of 5-HT to membranes more effectively (Ki=0.95 mM) than its uptake into vesicles (Ki=1.2mM) contrasting with D 1 which is a weaker inhibitor affecting vesicular uptake (Ki=2.5 mM) slightly more than membrane binding (Ki=3.1 mM). The results obtained suggest that, in addition to other mechanisms like receptor stimulation, 1-aminoadamantanes may act in parkinsonian patients by enriching the transmitter content in the synaptic cleft.</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="1978-09-11">Created</change><change when="1979-12-01">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/5CB6105AED86AF7058C521EEA6FC481340D26CD4/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</JournalTitle><JournalSubTitle>Basic neurosciences and genetics, Parkinson's disease and allied conditions, Alzheimer's disease and related disorders, biological psychiatry</JournalSubTitle><JournalAbbreviatedTitle>J. Neural Transmission</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Medicine & Public Health</JournalSubject><JournalSubject Type="Secondary">Pharmacology/Toxicology</JournalSubject><JournalSubject Type="Secondary">Neurology</JournalSubject><JournalSubject Type="Secondary">Psychiatry</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>44</VolumeIDStart><VolumeIDEnd>44</VolumeIDEnd><VolumeIssueCount>4</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>4</IssueIDStart><IssueIDEnd>4</IssueIDEnd><IssueArticleCount>10</IssueArticleCount><IssueHistory><CoverDate><DateString>1979</DateString><Year>1979</Year><Month>12</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1979</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art2"><ArticleInfo Language="En" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF01250322</ArticleID><ArticleDOI>10.1007/BF01250322</ArticleDOI><ArticleSequenceNumber>2</ArticleSequenceNumber><ArticleTitle Language="En">In vitro studies on the possible effects of 1-aminoadamantanes on the serotonergic system in M. Parkinson</ArticleTitle><ArticleFirstPage>263</ArticleFirstPage><ArticleLastPage>285</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2005</Year><Month>2</Month><Day>17</Day></RegistrationDate><Received><Year>1978</Year><Month>9</Month><Day>11</Day></Received></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1979</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>702</JournalID><VolumeIDStart>44</VolumeIDStart><VolumeIDEnd>44</VolumeIDEnd><IssueIDStart>4</IssueIDStart><IssueIDEnd>4</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" PresentAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>W.</GivenName><FamilyName>Wesemann</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1" PresentAffiliationID="Aff2"><AuthorName DisplayOrder="Western"><GivenName>G.</GivenName><FamilyName>Dette-Wildenhahn</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>H.</GivenName><FamilyName>Fellehner</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Abteilung für Neurodiemie, Physiologisch-chemisches Institut II</OrgDivision><OrgName>Philipps-Universität</OrgName><OrgAddress><City>Marburg/Lahn</City><Country>Federal Republic of Germany</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgName>c/o Behringwerke</OrgName><OrgAddress><Postcode>D-3550</Postcode><City>Marburg-Marbach</City><Country>Federal Republic of Germany</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Synaptosomes, synaptic vesicles, and membranes were isolated from rat brain homogenates by differential and density gradient centrifugation in sucrose. Synaptosomes incorporated serotonin (5-HT) with two different uptake mechanisms, high affinity: K<Subscript>t1</Subscript>=47 nM and low affinity: K<Subscript>t2</Subscript>=660 nM. Both uptake mechanisms are non-competitively inhibited by the potential antiparkinson drugs 1-aminoadamantane (amantadine, D 1: K<Subscript>i1</Subscript>=57<Emphasis Type="Italic">μ</Emphasis>M, K<Subscript>i2</Subscript>=96<Emphasis Type="Italic">μ</Emphasis>M) and 1-amino-3.5-dimethyladamantane (memantine, D 145: K<Subscript>i1</Subscript>=97<Emphasis Type="Italic">μ</Emphasis>M, K<Subscript>i2</Subscript>=150<Emphasis Type="Italic">μ</Emphasis>M). The incorporated 5-HT is released from Synaptosomes on incubation with high concentrations (0.5–5 mM) of the drugs or on electrical stimulation with rectangular pulses of alternating polarity. Subthreshold concentrations of these drugs (5–50<Emphasis Type="Italic">μ</Emphasis>M) which are too low to liberate 5-HT increase the electrically stimulated release of 5-HT.—The effect of D 1, D 145, and electrical stimulation on DA release parallels the results observed with 5-HT.</Para><Para>The uptake of 5-HT into isolated synaptic vesicles and the binding to isolated nerve ending membranes is non-competitively inhibited by 1-aminoadamantanes. D 145 inhibits the binding of 5-HT to membranes more effectively (K<Subscript>i</Subscript>=0.95 mM) than its uptake into vesicles (K<Subscript>i</Subscript>=1.2mM) contrasting with D 1 which is a weaker inhibitor affecting vesicular uptake (K<Subscript>i</Subscript>=2.5 mM) slightly more than membrane binding (K<Subscript>i</Subscript>=3.1 mM).</Para><Para>The results obtained suggest that, in addition to other mechanisms like receptor stimulation, 1-aminoadamantanes may act in parkinsonian patients by enriching the transmitter content in the synaptic cleft.</Para></Abstract></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>In vitro studies on the possible effects of 1-aminoadamantanes on the serotonergic system in M. Parkinson</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>In vitro studies on the possible effects of 1-aminoadamantanes on the serotonergic system in M. Parkinson</title></titleInfo><name type="personal"><namePart type="given">W.</namePart><namePart type="family">Wesemann</namePart><affiliation>Abteilung für Neurodiemie, Physiologisch-chemisches Institut II, Philipps-Universität, Marburg/Lahn, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Dette-Wildenhahn</namePart><affiliation>Abteilung für Neurodiemie, Physiologisch-chemisches Institut II, Philipps-Universität, Marburg/Lahn, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Fellehner</namePart><affiliation>Abteilung für Neurodiemie, Physiologisch-chemisches Institut II, Philipps-Universität, Marburg/Lahn, 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">1978-09-11</dateCreated><dateIssued encoding="w3cdtf">1979-12-01</dateIssued><copyrightDate encoding="w3cdtf">1979</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: Synaptosomes, synaptic vesicles, and membranes were isolated from rat brain homogenates by differential and density gradient centrifugation in sucrose. Synaptosomes incorporated serotonin (5-HT) with two different uptake mechanisms, high affinity: Kt1=47 nM and low affinity: Kt2=660 nM. Both uptake mechanisms are non-competitively inhibited by the potential antiparkinson drugs 1-aminoadamantane (amantadine, D 1: Ki1=57μM, Ki2=96μM) and 1-amino-3.5-dimethyladamantane (memantine, D 145: Ki1=97μM, Ki2=150μM). The incorporated 5-HT is released from Synaptosomes on incubation with high concentrations (0.5–5 mM) of the drugs or on electrical stimulation with rectangular pulses of alternating polarity. Subthreshold concentrations of these drugs (5–50μM) which are too low to liberate 5-HT increase the electrically stimulated release of 5-HT.—The effect of D 1, D 145, and electrical stimulation on DA release parallels the results observed with 5-HT. The uptake of 5-HT into isolated synaptic vesicles and the binding to isolated nerve ending membranes is non-competitively inhibited by 1-aminoadamantanes. D 145 inhibits the binding of 5-HT to membranes more effectively (Ki=0.95 mM) than its uptake into vesicles (Ki=1.2mM) contrasting with D 1 which is a weaker inhibitor affecting vesicular uptake (Ki=2.5 mM) slightly more than membrane binding (Ki=3.1 mM). The results obtained suggest that, in addition to other mechanisms like receptor stimulation, 1-aminoadamantanes may act in parkinsonian patients by enriching the transmitter content in the synaptic cleft.</abstract><relatedItem type="host"><titleInfo><title>Journal of Neural Transmission</title><subTitle>Basic neurosciences and genetics, Parkinson's disease and allied conditions, Alzheimer's disease and related disorders, biological psychiatry</subTitle></titleInfo><titleInfo type="abbreviated"><title>J. 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