5HT1A serotonin receptor agonists inhibit Plasmodium falciparum by blocking a membrane channel.
Identifieur interne : 000459 ( PubMed/Curation ); précédent : 000458; suivant : 0004605HT1A serotonin receptor agonists inhibit Plasmodium falciparum by blocking a membrane channel.
Auteurs : Christopher P. Locher [États-Unis] ; Peter C. Ruben ; Jiri Gut ; Philip J. RosenthalSource :
- Antimicrobial agents and chemotherapy [ 0066-4804 ] ; 2003.
Descripteurs français
- KwdFr :
- 7-Dipropylamino-5,6,7,8-tétrahydro-1-naphtol (pharmacologie), Agonistes des récepteurs de la sérotonine (pharmacologie), Animaux, Antisérotonines (pharmacologie), Buspirone (pharmacologie), Canaux ioniques (), Fibroblastes, Humains, Ligands, Lignée cellulaire, Membrane cellulaire (), Plasmodium falciparum (), Plasmodium falciparum (croissance et développement), Potentiels de membrane (), Relation dose-effet des médicaments, Récepteur de la sérotonine de type 5-HT1A (), Survie cellulaire (), Techniques de patch-clamp.
- MESH :
- croissance et développement : Plasmodium falciparum.
- pharmacologie : 7-Dipropylamino-5,6,7,8-tétrahydro-1-naphtol, Agonistes des récepteurs de la sérotonine, Antisérotonines, Buspirone.
- Animaux, Canaux ioniques, Fibroblastes, Humains, Ligands, Lignée cellulaire, Membrane cellulaire, Plasmodium falciparum, Potentiels de membrane, Relation dose-effet des médicaments, Récepteur de la sérotonine de type 5-HT1A, Survie cellulaire, Techniques de patch-clamp.
English descriptors
- KwdEn :
- 8-Hydroxy-2-(di-n-propylamino)tetralin (pharmacology), Animals, Buspirone (pharmacology), Cell Line, Cell Membrane (drug effects), Cell Survival (drug effects), Dose-Response Relationship, Drug, Fibroblasts, Humans, Ion Channels (drug effects), Ligands, Membrane Potentials (drug effects), Patch-Clamp Techniques, Plasmodium falciparum (drug effects), Plasmodium falciparum (growth & development), Receptor, Serotonin, 5-HT1A (drug effects), Serotonin Antagonists (pharmacology), Serotonin Receptor Agonists (pharmacology).
- MESH :
- chemical , drug effects : Ion Channels, Receptor, Serotonin, 5-HT1A.
- chemical , pharmacology : 8-Hydroxy-2-(di-n-propylamino)tetralin, Buspirone, Serotonin Antagonists, Serotonin Receptor Agonists.
- drug effects : Cell Membrane, Cell Survival, Membrane Potentials, Plasmodium falciparum.
- growth & development : Plasmodium falciparum.
- Animals, Cell Line, Dose-Response Relationship, Drug, Fibroblasts, Humans, Ligands, Patch-Clamp Techniques.
Abstract
To identify new leads for the treatment of Plasmodium falciparum malaria, we screened a panel of serotonin (5-hydroxytryptamine [5HT]) receptor agonists and antagonists and determined their effects on parasite growth. The 5HT1A receptor agonists 8-hydroxy-N-(di-n-propyl)-aminotetralin (8-OH-DPAT), 2,5-dimethoxy-4-iodoamphetamine, and 2,5-dimethoxy-4-bromophenylethylamine inhibited the growth of P. falciparum in vitro (50% inhibitory concentrations, 0.4, 0.7, and 1.5 microM, respectively). In further characterizing the antiparasitic effects of 8-OH-DPAT, we found that this serotonin receptor agonist did not affect the growth of Leishmania infantum, Trypanosoma cruzi, Trypanosoma brucei brucei, or Trichostrongylus colubriformis in vitro and did not demonstrate cytotoxicity against the human lung fibroblast cell line MRC-5. 8-OH-DPAT had similar levels of growth inhibition against several different P. falciparum isolates having distinct chemotherapeutic resistance phenotypes, and its antimalarial effect was additive when it was used in combination with chloroquine against a chloroquine-resistant isolate. In a patch clamp assay, 8-OH-DPAT blocked a P. falciparum surface membrane channel, suggesting that serotonin receptor agonists are a novel class of antimalarials that target a nutrient transport pathway. Since there may be neurological involvement with the use of 8-OH-DPAT and other serotonin receptor agonists in the treatment of falciparum malaria, new lead compounds derived from 8-OH-DPAT will need to be modified to prevent potential neurological side effects. Nevertheless, these results suggest that 8-OH-DPAT is a new lead compound with which to derive novel antimalarial agents and is a useful tool with which to characterize P. falciparum membrane channels.
DOI: 10.1128/aac.47.12.3806-3809.2003
PubMed: 14638487
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: Pour aller vers cette notice dans l'étape Curation :000459
Links to Exploration step
pubmed:14638487Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">5HT1A serotonin receptor agonists inhibit Plasmodium falciparum by blocking a membrane channel.</title><author><name sortKey="Locher, Christopher P" sort="Locher, Christopher P" uniqKey="Locher C" first="Christopher P" last="Locher">Christopher P. Locher</name><affiliation wicri:level="1"><nlm:affiliation>Department of Tropical Medicine and Medical Microbiology, John A Burns School of Medicine, University of Hawaii at Manoa, Honolulu, Hawaii 96816, USA. Christopher.locher@maxygen.com</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Tropical Medicine and Medical Microbiology, John A Burns School of Medicine, University of Hawaii at Manoa, Honolulu, Hawaii 96816</wicri:regionArea></affiliation></author><author><name sortKey="Ruben, Peter C" sort="Ruben, Peter C" uniqKey="Ruben P" first="Peter C" last="Ruben">Peter C. Ruben</name></author><author><name sortKey="Gut, Jiri" sort="Gut, Jiri" uniqKey="Gut J" first="Jiri" last="Gut">Jiri Gut</name></author><author><name sortKey="Rosenthal, Philip J" sort="Rosenthal, Philip J" uniqKey="Rosenthal P" first="Philip J" last="Rosenthal">Philip J. Rosenthal</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2003">2003</date><idno type="RBID">pubmed:14638487</idno><idno type="pmid">14638487</idno><idno type="doi">10.1128/aac.47.12.3806-3809.2003</idno><idno type="wicri:Area/PubMed/Corpus">000459</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000459</idno><idno type="wicri:Area/PubMed/Curation">000459</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000459</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">5HT1A serotonin receptor agonists inhibit Plasmodium falciparum by blocking a membrane channel.</title><author><name sortKey="Locher, Christopher P" sort="Locher, Christopher P" uniqKey="Locher C" first="Christopher P" last="Locher">Christopher P. Locher</name><affiliation wicri:level="1"><nlm:affiliation>Department of Tropical Medicine and Medical Microbiology, John A Burns School of Medicine, University of Hawaii at Manoa, Honolulu, Hawaii 96816, USA. Christopher.locher@maxygen.com</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Tropical Medicine and Medical Microbiology, John A Burns School of Medicine, University of Hawaii at Manoa, Honolulu, Hawaii 96816</wicri:regionArea></affiliation></author><author><name sortKey="Ruben, Peter C" sort="Ruben, Peter C" uniqKey="Ruben P" first="Peter C" last="Ruben">Peter C. Ruben</name></author><author><name sortKey="Gut, Jiri" sort="Gut, Jiri" uniqKey="Gut J" first="Jiri" last="Gut">Jiri Gut</name></author><author><name sortKey="Rosenthal, Philip J" sort="Rosenthal, Philip J" uniqKey="Rosenthal P" first="Philip J" last="Rosenthal">Philip J. Rosenthal</name></author></analytic><series><title level="j">Antimicrobial agents and chemotherapy</title><idno type="ISSN">0066-4804</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>8-Hydroxy-2-(di-n-propylamino)tetralin (pharmacology)</term><term>Animals</term><term>Buspirone (pharmacology)</term><term>Cell Line</term><term>Cell Membrane (drug effects)</term><term>Cell Survival (drug effects)</term><term>Dose-Response Relationship, Drug</term><term>Fibroblasts</term><term>Humans</term><term>Ion Channels (drug effects)</term><term>Ligands</term><term>Membrane Potentials (drug effects)</term><term>Patch-Clamp Techniques</term><term>Plasmodium falciparum (drug effects)</term><term>Plasmodium falciparum (growth & development)</term><term>Receptor, Serotonin, 5-HT1A (drug effects)</term><term>Serotonin Antagonists (pharmacology)</term><term>Serotonin Receptor Agonists (pharmacology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>7-Dipropylamino-5,6,7,8-tétrahydro-1-naphtol (pharmacologie)</term><term>Agonistes des récepteurs de la sérotonine (pharmacologie)</term><term>Animaux</term><term>Antisérotonines (pharmacologie)</term><term>Buspirone (pharmacologie)</term><term>Canaux ioniques ()</term><term>Fibroblastes</term><term>Humains</term><term>Ligands</term><term>Lignée cellulaire</term><term>Membrane cellulaire ()</term><term>Plasmodium falciparum ()</term><term>Plasmodium falciparum (croissance et développement)</term><term>Potentiels de membrane ()</term><term>Relation dose-effet des médicaments</term><term>Récepteur de la sérotonine de type 5-HT1A ()</term><term>Survie cellulaire ()</term><term>Techniques de patch-clamp</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Ion Channels</term><term>Receptor, Serotonin, 5-HT1A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>8-Hydroxy-2-(di-n-propylamino)tetralin</term><term>Buspirone</term><term>Serotonin Antagonists</term><term>Serotonin Receptor Agonists</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Plasmodium falciparum</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Membrane</term><term>Cell Survival</term><term>Membrane Potentials</term><term>Plasmodium falciparum</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Plasmodium falciparum</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>7-Dipropylamino-5,6,7,8-tétrahydro-1-naphtol</term><term>Agonistes des récepteurs de la sérotonine</term><term>Antisérotonines</term><term>Buspirone</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Dose-Response Relationship, Drug</term><term>Fibroblasts</term><term>Humans</term><term>Ligands</term><term>Patch-Clamp Techniques</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Canaux ioniques</term><term>Fibroblastes</term><term>Humains</term><term>Ligands</term><term>Lignée cellulaire</term><term>Membrane cellulaire</term><term>Plasmodium falciparum</term><term>Potentiels de membrane</term><term>Relation dose-effet des médicaments</term><term>Récepteur de la sérotonine de type 5-HT1A</term><term>Survie cellulaire</term><term>Techniques de patch-clamp</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To identify new leads for the treatment of Plasmodium falciparum malaria, we screened a panel of serotonin (5-hydroxytryptamine [5HT]) receptor agonists and antagonists and determined their effects on parasite growth. The 5HT1A receptor agonists 8-hydroxy-N-(di-n-propyl)-aminotetralin (8-OH-DPAT), 2,5-dimethoxy-4-iodoamphetamine, and 2,5-dimethoxy-4-bromophenylethylamine inhibited the growth of P. falciparum in vitro (50% inhibitory concentrations, 0.4, 0.7, and 1.5 microM, respectively). In further characterizing the antiparasitic effects of 8-OH-DPAT, we found that this serotonin receptor agonist did not affect the growth of Leishmania infantum, Trypanosoma cruzi, Trypanosoma brucei brucei, or Trichostrongylus colubriformis in vitro and did not demonstrate cytotoxicity against the human lung fibroblast cell line MRC-5. 8-OH-DPAT had similar levels of growth inhibition against several different P. falciparum isolates having distinct chemotherapeutic resistance phenotypes, and its antimalarial effect was additive when it was used in combination with chloroquine against a chloroquine-resistant isolate. In a patch clamp assay, 8-OH-DPAT blocked a P. falciparum surface membrane channel, suggesting that serotonin receptor agonists are a novel class of antimalarials that target a nutrient transport pathway. Since there may be neurological involvement with the use of 8-OH-DPAT and other serotonin receptor agonists in the treatment of falciparum malaria, new lead compounds derived from 8-OH-DPAT will need to be modified to prevent potential neurological side effects. Nevertheless, these results suggest that 8-OH-DPAT is a new lead compound with which to derive novel antimalarial agents and is a useful tool with which to characterize P. falciparum membrane channels.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">14638487</PMID><DateCompleted><Year>2004</Year><Month>01</Month><Day>13</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>09</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0066-4804</ISSN><JournalIssue CitedMedium="Print"><Volume>47</Volume><Issue>12</Issue><PubDate><Year>2003</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Antimicrobial agents and chemotherapy</Title><ISOAbbreviation>Antimicrob. Agents Chemother.</ISOAbbreviation></Journal><ArticleTitle>5HT1A serotonin receptor agonists inhibit Plasmodium falciparum by blocking a membrane channel.</ArticleTitle><Pagination><MedlinePgn>3806-9</MedlinePgn></Pagination><Abstract><AbstractText>To identify new leads for the treatment of Plasmodium falciparum malaria, we screened a panel of serotonin (5-hydroxytryptamine [5HT]) receptor agonists and antagonists and determined their effects on parasite growth. The 5HT1A receptor agonists 8-hydroxy-N-(di-n-propyl)-aminotetralin (8-OH-DPAT), 2,5-dimethoxy-4-iodoamphetamine, and 2,5-dimethoxy-4-bromophenylethylamine inhibited the growth of P. falciparum in vitro (50% inhibitory concentrations, 0.4, 0.7, and 1.5 microM, respectively). In further characterizing the antiparasitic effects of 8-OH-DPAT, we found that this serotonin receptor agonist did not affect the growth of Leishmania infantum, Trypanosoma cruzi, Trypanosoma brucei brucei, or Trichostrongylus colubriformis in vitro and did not demonstrate cytotoxicity against the human lung fibroblast cell line MRC-5. 8-OH-DPAT had similar levels of growth inhibition against several different P. falciparum isolates having distinct chemotherapeutic resistance phenotypes, and its antimalarial effect was additive when it was used in combination with chloroquine against a chloroquine-resistant isolate. In a patch clamp assay, 8-OH-DPAT blocked a P. falciparum surface membrane channel, suggesting that serotonin receptor agonists are a novel class of antimalarials that target a nutrient transport pathway. Since there may be neurological involvement with the use of 8-OH-DPAT and other serotonin receptor agonists in the treatment of falciparum malaria, new lead compounds derived from 8-OH-DPAT will need to be modified to prevent potential neurological side effects. Nevertheless, these results suggest that 8-OH-DPAT is a new lead compound with which to derive novel antimalarial agents and is a useful tool with which to characterize P. falciparum membrane channels.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Locher</LastName><ForeName>Christopher P</ForeName><Initials>CP</Initials><AffiliationInfo><Affiliation>Department of Tropical Medicine and Medical Microbiology, John A Burns School of Medicine, University of Hawaii at Manoa, Honolulu, Hawaii 96816, USA. Christopher.locher@maxygen.com</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ruben</LastName><ForeName>Peter C</ForeName><Initials>PC</Initials></Author><Author ValidYN="Y"><LastName>Gut</LastName><ForeName>Jiri</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Rosenthal</LastName><ForeName>Philip J</ForeName><Initials>PJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Antimicrob Agents Chemother</MedlineTA><NlmUniqueID>0315061</NlmUniqueID><ISSNLinking>0066-4804</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007473">Ion Channels</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008024">Ligands</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012702">Serotonin Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017366">Serotonin Receptor Agonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>112692-38-3</RegistryNumber><NameOfSubstance UI="D044282">Receptor, Serotonin, 5-HT1A</NameOfSubstance></Chemical><Chemical><RegistryNumber>78950-78-4</RegistryNumber><NameOfSubstance UI="D017371">8-Hydroxy-2-(di-n-propylamino)tetralin</NameOfSubstance></Chemical><Chemical><RegistryNumber>TK65WKS8HL</RegistryNumber><NameOfSubstance UI="D002065">Buspirone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017371" MajorTopicYN="N">8-Hydroxy-2-(di-n-propylamino)tetralin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002065" MajorTopicYN="N">Buspirone</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002462" MajorTopicYN="N">Cell Membrane</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004305" MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005347" MajorTopicYN="N">Fibroblasts</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007473" MajorTopicYN="N">Ion Channels</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008024" MajorTopicYN="N">Ligands</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008564" MajorTopicYN="N">Membrane Potentials</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018408" MajorTopicYN="N">Patch-Clamp Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010963" MajorTopicYN="N">Plasmodium falciparum</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D044282" MajorTopicYN="N">Receptor, Serotonin, 5-HT1A</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012702" MajorTopicYN="N">Serotonin Antagonists</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017366" MajorTopicYN="N">Serotonin Receptor Agonists</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2003</Year><Month>11</Month><Day>26</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2004</Year><Month>1</Month><Day>14</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2003</Year><Month>11</Month><Day>26</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">14638487</ArticleId><ArticleId IdType="pmc">PMC296210</ArticleId><ArticleId IdType="doi">10.1128/aac.47.12.3806-3809.2003</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Mol Biochem Parasitol. 2001 Oct;117(2):121-8</Citation><ArticleIdList><ArticleId IdType="pubmed">11606221</ArticleId></ArticleIdList></Reference><Reference><Citation>Anal Chem. 2001 Dec 1;73(23):5683-90</Citation><ArticleIdList><ArticleId IdType="pubmed">11774908</ArticleId></ArticleIdList></Reference><Reference><Citation>Mem Inst Oswaldo Cruz. 2001 Nov;96(8):1033-42</Citation><ArticleIdList><ArticleId IdType="pubmed">11784919</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet Infect Dis. 2002 Apr;2(4):209-18</Citation><ArticleIdList><ArticleId IdType="pubmed">11937421</ArticleId></ArticleIdList></Reference><Reference><Citation>Neurochem Int. 2003 Jul;43(2):155-64</Citation><ArticleIdList><ArticleId IdType="pubmed">12620284</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 1967 Jul 22;215(5099):437-9</Citation><ArticleIdList><ArticleId IdType="pubmed">4964555</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Trop Med Hyg. 1972 Jul;21(4):393-9</Citation><ArticleIdList><ArticleId IdType="pubmed">4559064</ArticleId></ArticleIdList></Reference><Reference><Citation>Life Sci. 1979 May 7;24(19):1813-22</Citation><ArticleIdList><ArticleId IdType="pubmed">459684</ArticleId></ArticleIdList></Reference><Reference><Citation>Antimicrob Agents Chemother. 1979 Dec;16(6):710-8</Citation><ArticleIdList><ArticleId IdType="pubmed">394674</ArticleId></ArticleIdList></Reference><Reference><Citation>Pflugers Arch. 1981 Aug;391(2):85-100</Citation><ArticleIdList><ArticleId IdType="pubmed">6270629</ArticleId></ArticleIdList></Reference><Reference><Citation>Trans R Soc Trop Med Hyg. 1983;77(2):228-31</Citation><ArticleIdList><ArticleId IdType="pubmed">6346591</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 1985 May;134(5):3439-44</Citation><ArticleIdList><ArticleId IdType="pubmed">3884711</ArticleId></ArticleIdList></Reference><Reference><Citation>J Med Chem. 1987 Jan;30(1):1-12</Citation><ArticleIdList><ArticleId IdType="pubmed">3543362</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Biochem Parasitol. 1987 Apr;23(3):193-201</Citation><ArticleIdList><ArticleId IdType="pubmed">3299083</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 1988 Dec 2;242(4883):1301-3</Citation><ArticleIdList><ArticleId IdType="pubmed">3057629</ArticleId></ArticleIdList></Reference><Reference><Citation>Trans R Soc Trop Med Hyg. 1990 Jul-Aug;84(4):474-8</Citation><ArticleIdList><ArticleId IdType="pubmed">2091331</ArticleId></ArticleIdList></Reference><Reference><Citation>J Ethnopharmacol. 1991 Apr;32(1-3):155-65</Citation><ArticleIdList><ArticleId IdType="pubmed">1881153</ArticleId></ArticleIdList></Reference><Reference><Citation>Trans R Soc Trop Med Hyg. 1992 May-Jun;86(3):235-6</Citation><ArticleIdList><ArticleId IdType="pubmed">1412641</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Trop Med Hyg. 1993 Feb;48(2):205-10</Citation><ArticleIdList><ArticleId IdType="pubmed">8447524</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 1993 Apr 15;362(6421):643-6</Citation><ArticleIdList><ArticleId IdType="pubmed">7681937</ArticleId></ArticleIdList></Reference><Reference><Citation>Antimicrob Agents Chemother. 1994 Jun;38(6):1419-21</Citation><ArticleIdList><ArticleId IdType="pubmed">8092848</ArticleId></ArticleIdList></Reference><Reference><Citation>Trans R Soc Trop Med Hyg. 1997 Nov-Dec;91(6):697-700</Citation><ArticleIdList><ArticleId IdType="pubmed">9509183</ArticleId></ArticleIdList></Reference><Reference><Citation>J Psychopharmacol. 1998;12(2):177-85</Citation><ArticleIdList><ArticleId IdType="pubmed">9694031</ArticleId></ArticleIdList></Reference><Reference><Citation>Eur J Pharmacol. 1999 Jan 8;364(2-3):123-32</Citation><ArticleIdList><ArticleId IdType="pubmed">9932714</ArticleId></ArticleIdList></Reference><Reference><Citation>Pharmacol Ther. 1999 Feb;81(2):91-110</Citation><ArticleIdList><ArticleId IdType="pubmed">10190581</ArticleId></ArticleIdList></Reference><Reference><Citation>J Psychopharmacol. 1999;13(1):100-9</Citation><ArticleIdList><ArticleId IdType="pubmed">10221364</ArticleId></ArticleIdList></Reference><Reference><Citation>J Ethnopharmacol. 1995 Nov 17;49(1):23-32</Citation><ArticleIdList><ArticleId IdType="pubmed">8786654</ArticleId></ArticleIdList></Reference><Reference><Citation>J Physiol. 2000 May 15;525 Pt 1:125-34</Citation><ArticleIdList><ArticleId IdType="pubmed">10811731</ArticleId></ArticleIdList></Reference><Reference><Citation>J Med Chem. 2000 Jul 13;43(14):2646-54</Citation><ArticleIdList><ArticleId IdType="pubmed">10893302</ArticleId></ArticleIdList></Reference><Reference><Citation>Medicine (Baltimore). 2000 Jul;79(4):201-9</Citation><ArticleIdList><ArticleId IdType="pubmed">10941349</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2000 Aug 31;406(6799):1001-5</Citation><ArticleIdList><ArticleId IdType="pubmed">10984055</ArticleId></ArticleIdList></Reference><Reference><Citation>Eur J Pharmacol. 2000 Oct 20;406(3):319-24</Citation><ArticleIdList><ArticleId IdType="pubmed">11040337</ArticleId></ArticleIdList></Reference><Reference><Citation>Pharmacol Toxicol. 2001 Feb;88(2):59-66</Citation><ArticleIdList><ArticleId IdType="pubmed">11169163</ArticleId></ArticleIdList></Reference><Reference><Citation>Physiol Rev. 2001 Apr;81(2):495-537</Citation><ArticleIdList><ArticleId IdType="pubmed">11274338</ArticleId></ArticleIdList></Reference><Reference><Citation>Antimicrob Agents Chemother. 2001 Sep;45(9):2655-7</Citation><ArticleIdList><ArticleId IdType="pubmed">11502547</ArticleId></ArticleIdList></Reference><Reference><Citation>Antimicrob Agents Chemother. 2001 Nov;45(11):3171-4</Citation><ArticleIdList><ArticleId IdType="pubmed">11600373</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/PubMed/Curation
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000459 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd -nk 000459 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= ChloroquineV1
|flux= PubMed
|étape= Curation
|type= RBID
|clé= pubmed:14638487
|texte= 5HT1A serotonin receptor agonists inhibit Plasmodium falciparum by blocking a membrane channel.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Curation/RBID.i -Sk "pubmed:14638487" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd \
| NlmPubMed2Wicri -a ChloroquineV1
| This area was generated with Dilib version V0.6.33. |  |