Effects of chronic oral administration of l-deprenyl in the dog
Identifieur interne : 002214 ( Istex/Corpus ); précédent : 002213; suivant : 002215Effects of chronic oral administration of l-deprenyl in the dog
Auteurs : N. W Milgram ; G. O Ivy ; M. P Murphy ; E. Head ; P. H Wu ; W. W Ruehl ; P. H Yu ; D. A Durden ; B. A Davis ; A. A BoultonSource :
- Pharmacology, Biochemistry and Behavior [ 0091-3057 ] ; 1995.
Abstract
Dogs were administered capsules containing l-deprenyl daily over 3 weeks at dose levels of 0, 0.1, 0.5, and 1.0 mg/kg. Spontaneous behavior was measured using a canine open field test, and was not significantly affected by l-deprenyl. Plasma levels of amphetamine showed a clear dose-dependent elevation 2 h following treatment, but were markedly lower after 24 h, and were undetectable 5 days following the last treatment. Plasma levels of phenylethylamine were increased, but were highly variable. Animals sacrificed 1 day following the last treatment showed a dose-dependent inhibition of monoamine oxidase B in the brain, liver, and kidney, whereas monoamine oxidase A was unaffected in these tissues. l-Deprenyl also caused an increase in phenylethylamine in the striatum and hypothalamus, but not in the neocortex. Brain levels of DA, DOPAC, 3-MT, HVA, 5-HT, and 5-HIAA were unaffected. The pharmacological profile for the dog is distinct from that of other species in that long-term treatment did not produce any significant inhibition of MAO-A activity. The absence of an effect on biogenic amines or metabolites suggests that the metabolism of dopamine is mediated at least in part through pathways other than MAO-B in the normal adult dog.
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DOI: 10.1016/0091-3057(94)00417-H
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P Murphy</name><affiliation><mods:affiliation>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</mods:affiliation></affiliation></author><author><name sortKey="Head, E" sort="Head, E" uniqKey="Head E" first="E" last="Head">E. Head</name><affiliation><mods:affiliation>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</mods:affiliation></affiliation></author><author><name sortKey="Wu, P H" sort="Wu, P H" uniqKey="Wu P" first="P. H" last="Wu">P. H Wu</name><affiliation><mods:affiliation>Department of Pharmacology, University of Toronto, Toronto, Ontario Canada</mods:affiliation></affiliation></author><author><name sortKey="Ruehl, W W" sort="Ruehl, W W" uniqKey="Ruehl W" first="W. W" last="Ruehl">W. 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W Milgram</name><affiliation><mods:affiliation>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</mods:affiliation></affiliation></author><author><name sortKey="Ivy, G O" sort="Ivy, G O" uniqKey="Ivy G" first="G. O" last="Ivy">G. O Ivy</name><affiliation><mods:affiliation>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</mods:affiliation></affiliation></author><author><name sortKey="Murphy, M P" sort="Murphy, M P" uniqKey="Murphy M" first="M. P" last="Murphy">M. P Murphy</name><affiliation><mods:affiliation>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</mods:affiliation></affiliation></author><author><name sortKey="Head, E" sort="Head, E" uniqKey="Head E" first="E" last="Head">E. Head</name><affiliation><mods:affiliation>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</mods:affiliation></affiliation></author><author><name sortKey="Wu, P H" sort="Wu, P H" uniqKey="Wu P" first="P. H" last="Wu">P. H Wu</name><affiliation><mods:affiliation>Department of Pharmacology, University of Toronto, Toronto, Ontario Canada</mods:affiliation></affiliation></author><author><name sortKey="Ruehl, W W" sort="Ruehl, W W" uniqKey="Ruehl W" first="W. W" last="Ruehl">W. W Ruehl</name><affiliation><mods:affiliation>Deprenyl Animal Health Inc., Overland Park, KS Canada</mods:affiliation></affiliation></author><author><name sortKey="Yu, P H" sort="Yu, P H" uniqKey="Yu P" first="P. H" last="Yu">P. H Yu</name><affiliation><mods:affiliation>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</mods:affiliation></affiliation></author><author><name sortKey="Durden, D A" sort="Durden, D A" uniqKey="Durden D" first="D. A" last="Durden">D. A Durden</name><affiliation><mods:affiliation>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</mods:affiliation></affiliation></author><author><name sortKey="Davis, B A" sort="Davis, B A" uniqKey="Davis B" first="B. A" last="Davis">B. A Davis</name><affiliation><mods:affiliation>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</mods:affiliation></affiliation></author><author><name sortKey="Boulton, A A" sort="Boulton, A A" uniqKey="Boulton A" first="A. A" last="Boulton">A. A Boulton</name><affiliation><mods:affiliation>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Pharmacology, Biochemistry and Behavior</title><title level="j" type="abbrev">PBB</title><idno type="ISSN">0091-3057</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995">1995</date><biblScope unit="volume">51</biblScope><biblScope unit="issue">2–3</biblScope><biblScope unit="page" from="421">421</biblScope><biblScope unit="page" to="428">428</biblScope></imprint><idno type="ISSN">0091-3057</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0091-3057</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dogs were administered capsules containing l-deprenyl daily over 3 weeks at dose levels of 0, 0.1, 0.5, and 1.0 mg/kg. Spontaneous behavior was measured using a canine open field test, and was not significantly affected by l-deprenyl. Plasma levels of amphetamine showed a clear dose-dependent elevation 2 h following treatment, but were markedly lower after 24 h, and were undetectable 5 days following the last treatment. Plasma levels of phenylethylamine were increased, but were highly variable. Animals sacrificed 1 day following the last treatment showed a dose-dependent inhibition of monoamine oxidase B in the brain, liver, and kidney, whereas monoamine oxidase A was unaffected in these tissues. l-Deprenyl also caused an increase in phenylethylamine in the striatum and hypothalamus, but not in the neocortex. Brain levels of DA, DOPAC, 3-MT, HVA, 5-HT, and 5-HIAA were unaffected. The pharmacological profile for the dog is distinct from that of other species in that long-term treatment did not produce any significant inhibition of MAO-A activity. The absence of an effect on biogenic amines or metabolites suggests that the metabolism of dopamine is mediated at least in part through pathways other than MAO-B in the normal adult dog.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>N.W Milgram</name><affiliations><json:string>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</json:string></affiliations></json:item><json:item><name>G.O Ivy</name><affiliations><json:string>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</json:string></affiliations></json:item><json:item><name>M.P Murphy</name><affiliations><json:string>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</json:string></affiliations></json:item><json:item><name>E Head</name><affiliations><json:string>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</json:string></affiliations></json:item><json:item><name>P.H Wu</name><affiliations><json:string>Department of Pharmacology, University of Toronto, Toronto, Ontario Canada</json:string></affiliations></json:item><json:item><name>W.W Ruehl</name><affiliations><json:string>Deprenyl Animal Health Inc., Overland Park, KS Canada</json:string></affiliations></json:item><json:item><name>P.H Yu</name><affiliations><json:string>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</json:string></affiliations></json:item><json:item><name>D.A Durden</name><affiliations><json:string>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</json:string></affiliations></json:item><json:item><name>B.A Davis</name><affiliations><json:string>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</json:string></affiliations></json:item><json:item><name>A.A Boulton</name><affiliations><json:string>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>l-Deprenyl</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dog</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Monoamine oxidase A</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Monoamine oxidase B</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Phenylethylamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Amphetamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Monoamines</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Monoamine metabolites</value></json:item></subject><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Dogs were administered capsules containing l-deprenyl daily over 3 weeks at dose levels of 0, 0.1, 0.5, and 1.0 mg/kg. Spontaneous behavior was measured using a canine open field test, and was not significantly affected by l-deprenyl. Plasma levels of amphetamine showed a clear dose-dependent elevation 2 h following treatment, but were markedly lower after 24 h, and were undetectable 5 days following the last treatment. Plasma levels of phenylethylamine were increased, but were highly variable. Animals sacrificed 1 day following the last treatment showed a dose-dependent inhibition of monoamine oxidase B in the brain, liver, and kidney, whereas monoamine oxidase A was unaffected in these tissues. l-Deprenyl also caused an increase in phenylethylamine in the striatum and hypothalamus, but not in the neocortex. Brain levels of DA, DOPAC, 3-MT, HVA, 5-HT, and 5-HIAA were unaffected. The pharmacological profile for the dog is distinct from that of other species in that long-term treatment did not produce any significant inhibition of MAO-A activity. The absence of an effect on biogenic amines or metabolites suggests that the metabolism of dopamine is mediated at least in part through pathways other than MAO-B in the normal adult dog.</abstract><qualityIndicators><score>7.18</score><pdfWordCount>4852</pdfWordCount><pdfCharCount>30173</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>8</pdfPageCount><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>194</abstractWordCount><abstractCharCount>1249</abstractCharCount><keywordCount>8</keywordCount></qualityIndicators><title>Effects of chronic oral administration of l-deprenyl in the dog</title><pii><json:string>0091-3057(94)00417-H</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Advances in biochemical psychopharmacology</title><language><json:string>unknown</json:string></language><volume>vol. 5</volume><pages><first>355</first><last>370</last></pages></serie><host><title>Pharmacology, Biochemistry and Behavior</title><language><json:string>unknown</json:string></language><publicationDate>1995</publicationDate><issn><json:string>0091-3057</json:string></issn><pii><json:string>S0091-3057(00)X0013-5</json:string></pii><volume>51</volume><issue>2–3</issue><pages><first>421</first><last>428</last></pages><genre><json:string>journal</json:string></genre></host><categories><wos><json:string>science</json:string><json:string>pharmacology & pharmacy</json:string><json:string>neurosciences</json:string><json:string>behavioral sciences</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & neurosurgery</json:string></scienceMetrix><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences medicales</json:string></inist></categories><publicationDate>1995</publicationDate><copyrightDate>1995</copyrightDate><doi><json:string>10.1016/0091-3057(94)00417-H</json:string></doi><id>A30110B5198986F739340EB8596571EBF803C2E9</id><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api-v5.istex.fr/document/A30110B5198986F739340EB8596571EBF803C2E9/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api-v5.istex.fr/document/A30110B5198986F739340EB8596571EBF803C2E9/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api-v5.istex.fr/document/A30110B5198986F739340EB8596571EBF803C2E9/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Effects of chronic oral administration of l-deprenyl in the dog</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>1995</date></publicationStmt><notesStmt><note type="content">Section title: Article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Effects of chronic oral administration of l-deprenyl in the dog</title><author xml:id="author-0000"><persName><forename type="first">N.W</forename><surname>Milgram</surname></persName><note type="biography">Requests for reprints should be addressed to N.W. Milgram, Life Sciences Division, Scarborough Campus, University of Toronto, 1265 Military Trail, Scarborough, Ontario M1C 1A4 Canada.</note><affiliation>Requests for reprints should be addressed to N.W. Milgram, Life Sciences Division, Scarborough Campus, University of Toronto, 1265 Military Trail, Scarborough, Ontario M1C 1A4 Canada.</affiliation><affiliation>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</affiliation></author><author xml:id="author-0001"><persName><forename type="first">G.O</forename><surname>Ivy</surname></persName><affiliation>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</affiliation></author><author xml:id="author-0002"><persName><forename type="first">M.P</forename><surname>Murphy</surname></persName><affiliation>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</affiliation></author><author xml:id="author-0003"><persName><forename type="first">E</forename><surname>Head</surname></persName><affiliation>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</affiliation></author><author xml:id="author-0004"><persName><forename type="first">P.H</forename><surname>Wu</surname></persName><affiliation>Department of Pharmacology, University of Toronto, Toronto, Ontario Canada</affiliation></author><author xml:id="author-0005"><persName><forename type="first">W.W</forename><surname>Ruehl</surname></persName><affiliation>Deprenyl Animal Health Inc., Overland Park, KS Canada</affiliation></author><author xml:id="author-0006"><persName><forename type="first">P.H</forename><surname>Yu</surname></persName><affiliation>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</affiliation></author><author xml:id="author-0007"><persName><forename type="first">D.A</forename><surname>Durden</surname></persName><affiliation>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</affiliation></author><author xml:id="author-0008"><persName><forename type="first">B.A</forename><surname>Davis</surname></persName><affiliation>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</affiliation></author><author xml:id="author-0009"><persName><forename type="first">A.A</forename><surname>Boulton</surname></persName><affiliation>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</affiliation></author><idno type="istex">A30110B5198986F739340EB8596571EBF803C2E9</idno><idno type="DOI">10.1016/0091-3057(94)00417-H</idno><idno type="PII">0091-3057(94)00417-H</idno></analytic><monogr><title level="j">Pharmacology, Biochemistry and Behavior</title><title level="j" type="abbrev">PBB</title><idno type="pISSN">0091-3057</idno><idno type="PII">S0091-3057(00)X0013-5</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995"></date><biblScope unit="volume">51</biblScope><biblScope unit="issue">2–3</biblScope><biblScope unit="page" from="421">421</biblScope><biblScope unit="page" to="428">428</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1995</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Dogs were administered capsules containing l-deprenyl daily over 3 weeks at dose levels of 0, 0.1, 0.5, and 1.0 mg/kg. Spontaneous behavior was measured using a canine open field test, and was not significantly affected by l-deprenyl. Plasma levels of amphetamine showed a clear dose-dependent elevation 2 h following treatment, but were markedly lower after 24 h, and were undetectable 5 days following the last treatment. Plasma levels of phenylethylamine were increased, but were highly variable. Animals sacrificed 1 day following the last treatment showed a dose-dependent inhibition of monoamine oxidase B in the brain, liver, and kidney, whereas monoamine oxidase A was unaffected in these tissues. l-Deprenyl also caused an increase in phenylethylamine in the striatum and hypothalamus, but not in the neocortex. Brain levels of DA, DOPAC, 3-MT, HVA, 5-HT, and 5-HIAA were unaffected. The pharmacological profile for the dog is distinct from that of other species in that long-term treatment did not produce any significant inhibition of MAO-A activity. The absence of an effect on biogenic amines or metabolites suggests that the metabolism of dopamine is mediated at least in part through pathways other than MAO-B in the normal adult dog.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>l-Deprenyl</term></item><item><term>Dog</term></item><item><term>Monoamine oxidase A</term></item><item><term>Monoamine oxidase B</term></item><item><term>Phenylethylamine</term></item><item><term>Amphetamine</term></item><item><term>Monoamines</term></item><item><term>Monoamine metabolites</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/A30110B5198986F739340EB8596571EBF803C2E9/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: 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:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>PBB</jid><aid>9400417H</aid><ce:pii>0091-3057(94)00417-H</ce:pii><ce:doi>10.1016/0091-3057(94)00417-H</ce:doi><ce:copyright type="unknown" year="1995"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Article</ce:textfn></ce:dochead><ce:title>Effects of chronic oral administration of <ce:small-caps>l</ce:small-caps>-deprenyl in the dog</ce:title><ce:author-group><ce:author><ce:given-name>N.W</ce:given-name><ce:surname>Milgram</ce:surname><ce:cross-ref refid="COR1"><ce:sup>1</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>G.O</ce:given-name><ce:surname>Ivy</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>M.P</ce:given-name><ce:surname>Murphy</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>E</ce:given-name><ce:surname>Head</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>P.H</ce:given-name><ce:surname>Wu</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>†</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>W.W</ce:given-name><ce:surname>Ruehl</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>‡</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>P.H</ce:given-name><ce:surname>Yu</ce:surname><ce:cross-ref refid="AFF4"><ce:sup>§</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>D.A</ce:given-name><ce:surname>Durden</ce:surname><ce:cross-ref refid="AFF4"><ce:sup>§</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>B.A</ce:given-name><ce:surname>Davis</ce:surname><ce:cross-ref refid="AFF4"><ce:sup>§</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>A.A</ce:given-name><ce:surname>Boulton</ce:surname><ce:cross-ref refid="AFF4"><ce:sup>§</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Pharmacology, University of Toronto, Toronto, Ontario Canada</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Deprenyl Animal Health Inc., Overland Park, KS Canada</ce:textfn></ce:affiliation><ce:affiliation id="AFF4"><ce:label>d</ce:label><ce:textfn>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>1</ce:label><ce:text>Requests for reprints should be addressed to N.W. Milgram, Life Sciences Division, Scarborough Campus, University of Toronto, 1265 Military Trail, Scarborough, Ontario M1C 1A4 Canada.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="16" month="3" year="1994"></ce:date-received><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Dogs were administered capsules containing <ce:small-caps>l</ce:small-caps>-deprenyl daily over 3 weeks at dose levels of 0, 0.1, 0.5, and 1.0 mg/kg. Spontaneous behavior was measured using a canine open field test, and was not significantly affected by <ce:small-caps>l</ce:small-caps>-deprenyl. Plasma levels of amphetamine showed a clear dose-dependent elevation 2 h following treatment, but were markedly lower after 24 h, and were undetectable 5 days following the last treatment. Plasma levels of phenylethylamine were increased, but were highly variable. Animals sacrificed 1 day following the last treatment showed a dose-dependent inhibition of monoamine oxidase B in the brain, liver, and kidney, whereas monoamine oxidase A was unaffected in these tissues. <ce:small-caps>l</ce:small-caps>-Deprenyl also caused an increase in phenylethylamine in the striatum and hypothalamus, but not in the neocortex. Brain levels of DA, DOPAC, 3-MT, HVA, 5-HT, and 5-HIAA were unaffected. The pharmacological profile for the dog is distinct from that of other species in that long-term treatment did not produce any significant inhibition of MAO-A activity. The absence of an effect on biogenic amines or metabolites suggests that the metabolism of dopamine is mediated at least in part through pathways other than MAO-B in the normal adult dog.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text><ce:small-caps>l</ce:small-caps>-Deprenyl</ce:text></ce:keyword><ce:keyword><ce:text>Dog</ce:text></ce:keyword><ce:keyword><ce:text>Monoamine oxidase A</ce:text></ce:keyword><ce:keyword><ce:text>Monoamine oxidase B</ce:text></ce:keyword><ce:keyword><ce:text>Phenylethylamine</ce:text></ce:keyword><ce:keyword><ce:text>Amphetamine</ce:text></ce:keyword><ce:keyword><ce:text>Monoamines</ce:text></ce:keyword><ce:keyword><ce:text>Monoamine metabolites</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Effects of chronic oral administration of l-deprenyl in the dog</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Effects of chronic oral administration of</title></titleInfo><name type="personal"><namePart type="given">N.W</namePart><namePart type="family">Milgram</namePart><affiliation>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</affiliation><description>Requests for reprints should be addressed to N.W. Milgram, Life Sciences Division, Scarborough Campus, University of Toronto, 1265 Military Trail, Scarborough, Ontario M1C 1A4 Canada.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.O</namePart><namePart type="family">Ivy</namePart><affiliation>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.P</namePart><namePart type="family">Murphy</namePart><affiliation>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Head</namePart><affiliation>Life Sciences Division, Scarborough Campus, University of Toronto, Scarborough, Ontario Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.H</namePart><namePart type="family">Wu</namePart><affiliation>Department of Pharmacology, University of Toronto, Toronto, Ontario Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.W</namePart><namePart type="family">Ruehl</namePart><affiliation>Deprenyl Animal Health Inc., Overland Park, KS Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.H</namePart><namePart type="family">Yu</namePart><affiliation>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D.A</namePart><namePart type="family">Durden</namePart><affiliation>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B.A</namePart><namePart type="family">Davis</namePart><affiliation>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.A</namePart><namePart type="family">Boulton</namePart><affiliation>Neuropsychiatric Research, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1995</dateIssued><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Dogs were administered capsules containing l-deprenyl daily over 3 weeks at dose levels of 0, 0.1, 0.5, and 1.0 mg/kg. Spontaneous behavior was measured using a canine open field test, and was not significantly affected by l-deprenyl. Plasma levels of amphetamine showed a clear dose-dependent elevation 2 h following treatment, but were markedly lower after 24 h, and were undetectable 5 days following the last treatment. Plasma levels of phenylethylamine were increased, but were highly variable. Animals sacrificed 1 day following the last treatment showed a dose-dependent inhibition of monoamine oxidase B in the brain, liver, and kidney, whereas monoamine oxidase A was unaffected in these tissues. l-Deprenyl also caused an increase in phenylethylamine in the striatum and hypothalamus, but not in the neocortex. Brain levels of DA, DOPAC, 3-MT, HVA, 5-HT, and 5-HIAA were unaffected. The pharmacological profile for the dog is distinct from that of other species in that long-term treatment did not produce any significant inhibition of MAO-A activity. The absence of an effect on biogenic amines or metabolites suggests that the metabolism of dopamine is mediated at least in part through pathways other than MAO-B in the normal adult dog.</abstract><note type="content">Section title: Article</note><subject><genre>Keywords</genre><topic>l-Deprenyl</topic><topic>Dog</topic><topic>Monoamine oxidase A</topic><topic>Monoamine oxidase B</topic><topic>Phenylethylamine</topic><topic>Amphetamine</topic><topic>Monoamines</topic><topic>Monoamine metabolites</topic></subject><relatedItem type="host"><titleInfo><title>Pharmacology, Biochemistry and Behavior</title></titleInfo><titleInfo type="abbreviated"><title>PBB</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">199506</dateIssued></originInfo><identifier type="ISSN">0091-3057</identifier><identifier type="PII">S0091-3057(00)X0013-5</identifier><part><date>199506</date><detail type="volume"><number>51</number><caption>vol.</caption></detail><detail type="issue"><number>2–3</number><caption>no.</caption></detail><extent unit="issue pages"><start>165</start><end>564</end></extent><extent unit="pages"><start>421</start><end>428</end></extent></part></relatedItem><identifier type="istex">A30110B5198986F739340EB8596571EBF803C2E9</identifier><identifier type="DOI">10.1016/0091-3057(94)00417-H</identifier><identifier type="PII">0091-3057(94)00417-H</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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