AutomedicationFrancoV1, Main, Exploration, bibRecord, 000988

Decrease of cocaine, but not heroin, self-administration and relapse by the tyrosine kinase inhibitor masitinib in male Sprague Dawley rats.

Identifieur interne : 000988 ( Main/Exploration ); précédent : 000987; suivant : 000989

Decrease of cocaine, but not heroin, self-administration and relapse by the tyrosine kinase inhibitor masitinib in male Sprague Dawley rats.

Auteurs : A. Belin-Rauscent [Royaume-Uni] ; J. Lacoste [France] ; O. Hermine [France] ; A. Moussy [France] ; B J Everitt [Royaume-Uni] ; David Belin [Royaume-Uni]

Source :

Psychopharmacology [ 1432-2072 ] ; 2018.

RBID : pubmed:29520592

Descripteurs français

KwdFr :
- Administration par voie orale (MeSH), Analgésiques morphiniques (administration et posologie), Animaux (MeSH), Autoadministration (MeSH), Cocaïne (administration et posologie), Comportement toxicomaniaque (psychologie), Comportement toxicomaniaque (traitement médicamenteux), Conditionnement opérant (effets des médicaments et des substances chimiques), Conditionnement opérant (physiologie), Héroïne (administration et posologie), Inhibiteurs de la capture de la dopamine (administration et posologie), Inhibiteurs de protéines kinases (administration et posologie), Motivation (effets des médicaments et des substances chimiques), Motivation (physiologie), Mâle (MeSH), Rat Sprague-Dawley (MeSH), Rats (MeSH), Récidive (MeSH), Thiazoles (administration et posologie).
MESH :
- administration et posologie : Analgésiques morphiniques, Cocaïne, Héroïne, Inhibiteurs de la capture de la dopamine, Inhibiteurs de protéines kinases, Thiazoles.
- effets des médicaments et des substances chimiques : Conditionnement opérant, Motivation.
- physiologie : Conditionnement opérant, Motivation.
- psychologie : Comportement toxicomaniaque.
- traitement médicamenteux : Comportement toxicomaniaque.
- Administration par voie orale, Animaux, Autoadministration, Mâle, Rat Sprague-Dawley, Rats, Récidive.

English descriptors

KwdEn :
- Administration, Oral (MeSH), Analgesics, Opioid (administration & dosage), Animals (MeSH), Behavior, Addictive (drug therapy), Behavior, Addictive (psychology), Cocaine (administration & dosage), Conditioning, Operant (drug effects), Conditioning, Operant (physiology), Dopamine Uptake Inhibitors (administration & dosage), Heroin (administration & dosage), Male (MeSH), Motivation (drug effects), Motivation (physiology), Protein Kinase Inhibitors (administration & dosage), Rats (MeSH), Rats, Sprague-Dawley (MeSH), Recurrence (MeSH), Reinforcement, Psychology (MeSH), Self Administration (MeSH), Thiazoles (administration & dosage).
MESH :
- chemical , administration & dosage : Analgesics, Opioid, Cocaine, Dopamine Uptake Inhibitors, Heroin, Protein Kinase Inhibitors, Thiazoles.
- drug effects : Conditioning, Operant, Motivation.
- drug therapy : Behavior, Addictive.
- physiology : Conditioning, Operant, Motivation.
- psychology : Behavior, Addictive.
- Administration, Oral, Animals, Male, Rats, Rats, Sprague-Dawley, Recurrence, Reinforcement, Psychology, Self Administration.

Abstract

RATIONALE

Accumulating evidence shows that cocaine, and also heroin, influence several tyrosine kinases, expressed in neurons and in non-neuronal populations such as microglia, astrocytes and mast-cells. Drug-induced activation of mast cells both triggers inflammatory processes in the brain mediated by the glial cells they activate, and facilitates histamine release which may directly influence the dopamine system. Thus, by triggering the activation and degranulation of mast cells dependent on the tyrosine kinase c-kit and Fyn, the latter being also involved in NMDA-dependent synaptic plasticity, cocaine and heroin may indirectly influence the neural mechanisms that mediate their reinforcing properties. Masitinib, a novel tyrosine kinase inhibitor with high selectivity for c-Kit, Fyn and Lyn, may alter the aberrant consequences of the activation of these tyrosine kinases by cocaine and heroin.

OBJECTIVE

We investigated in rats the effect of a chronic oral treatment with masitinib (20 mg/kg) on the reinforcing and motivational properties of self-administered cocaine (250 μg/infusion) and heroin (40 μg/infusion).

METHODS

Three different cohorts of rats were trained instrumentally to respond for cocaine, heroin or food under continuous reinforcement. In each group, we assessed the influence of chronic daily treatment with masitinib on the maintenance of instrumental responding and intake and the motivation for the reinforcer. Thus, masitinib and vehicle-treated rats were challenged to adapt to high behavioural demand, to respond under a progressive ratio schedule of reinforcement and to reinstate instrumental responding after extinction and/or abstinence.

RESULTS

Masitinib selectively decreased cocaine intake, the motivation for cocaine and the subsequent propensity to respond for cocaine under extinction, while having no effect on instrumental responding for heroin or food.

CONCLUSION

The present findings suggest masitinib, a drug with proven efficacy in CNS disorders, could represent a novel treatment for cocaine addiction provided its influence on the reinforcing and incentive properties of the drug is confirmed.

DOI: 10.1007/s00213-018-4865-0
PubMed: 29520592
PubMed Central: PMC5920000

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<term>Analgesics, Opioid (administration & dosage)</term>
<term>Animals (MeSH)</term>
<term>Behavior, Addictive (drug therapy)</term>
<term>Behavior, Addictive (psychology)</term>
<term>Cocaine (administration & dosage)</term>
<term>Conditioning, Operant (drug effects)</term>
<term>Conditioning, Operant (physiology)</term>
<term>Dopamine Uptake Inhibitors (administration & dosage)</term>
<term>Heroin (administration & dosage)</term>
<term>Male (MeSH)</term>
<term>Motivation (drug effects)</term>
<term>Motivation (physiology)</term>
<term>Protein Kinase Inhibitors (administration & dosage)</term>
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<term>Rats, Sprague-Dawley (MeSH)</term>
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<term>Self Administration (MeSH)</term>
<term>Thiazoles (administration & dosage)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Administration par voie orale (MeSH)</term>
<term>Analgésiques morphiniques (administration et posologie)</term>
<term>Animaux (MeSH)</term>
<term>Autoadministration (MeSH)</term>
<term>Cocaïne (administration et posologie)</term>
<term>Comportement toxicomaniaque (psychologie)</term>
<term>Comportement toxicomaniaque (traitement médicamenteux)</term>
<term>Conditionnement opérant (effets des médicaments et des substances chimiques)</term>
<term>Conditionnement opérant (physiologie)</term>
<term>Héroïne (administration et posologie)</term>
<term>Inhibiteurs de la capture de la dopamine (administration et posologie)</term>
<term>Inhibiteurs de protéines kinases (administration et posologie)</term>
<term>Motivation (effets des médicaments et des substances chimiques)</term>
<term>Motivation (physiologie)</term>
<term>Mâle (MeSH)</term>
<term>Rat Sprague-Dawley (MeSH)</term>
<term>Rats (MeSH)</term>
<term>Récidive (MeSH)</term>
<term>Thiazoles (administration et posologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Analgesics, Opioid</term>
<term>Cocaine</term>
<term>Dopamine Uptake Inhibitors</term>
<term>Heroin</term>
<term>Protein Kinase Inhibitors</term>
<term>Thiazoles</term>
</keywords>
<keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Analgésiques morphiniques</term>
<term>Cocaïne</term>
<term>Héroïne</term>
<term>Inhibiteurs de la capture de la dopamine</term>
<term>Inhibiteurs de protéines kinases</term>
<term>Thiazoles</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Conditioning, Operant</term>
<term>Motivation</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Behavior, Addictive</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Conditionnement opérant</term>
<term>Motivation</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Conditionnement opérant</term>
<term>Motivation</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Conditioning, Operant</term>
<term>Motivation</term>
</keywords>
<keywords scheme="MESH" qualifier="psychologie" xml:lang="fr"><term>Comportement toxicomaniaque</term>
</keywords>
<keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Behavior, Addictive</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Comportement toxicomaniaque</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Administration, Oral</term>
<term>Animals</term>
<term>Male</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Recurrence</term>
<term>Reinforcement, Psychology</term>
<term>Self Administration</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Administration par voie orale</term>
<term>Animaux</term>
<term>Autoadministration</term>
<term>Mâle</term>
<term>Rat Sprague-Dawley</term>
<term>Rats</term>
<term>Récidive</term>
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<front><div type="abstract" xml:lang="en"><p><b>RATIONALE</b>
</p>
<p>Accumulating evidence shows that cocaine, and also heroin, influence several tyrosine kinases, expressed in neurons and in non-neuronal populations such as microglia, astrocytes and mast-cells. Drug-induced activation of mast cells both triggers inflammatory processes in the brain mediated by the glial cells they activate, and facilitates histamine release which may directly influence the dopamine system. Thus, by triggering the activation and degranulation of mast cells dependent on the tyrosine kinase c-kit and Fyn, the latter being also involved in NMDA-dependent synaptic plasticity, cocaine and heroin may indirectly influence the neural mechanisms that mediate their reinforcing properties. Masitinib, a novel tyrosine kinase inhibitor with high selectivity for c-Kit, Fyn and Lyn, may alter the aberrant consequences of the activation of these tyrosine kinases by cocaine and heroin.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>OBJECTIVE</b>
</p>
<p>We investigated in rats the effect of a chronic oral treatment with masitinib (20 mg/kg) on the reinforcing and motivational properties of self-administered cocaine (250 μg/infusion) and heroin (40 μg/infusion).</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS</b>
</p>
<p>Three different cohorts of rats were trained instrumentally to respond for cocaine, heroin or food under continuous reinforcement. In each group, we assessed the influence of chronic daily treatment with masitinib on the maintenance of instrumental responding and intake and the motivation for the reinforcer. Thus, masitinib and vehicle-treated rats were challenged to adapt to high behavioural demand, to respond under a progressive ratio schedule of reinforcement and to reinstate instrumental responding after extinction and/or abstinence.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>Masitinib selectively decreased cocaine intake, the motivation for cocaine and the subsequent propensity to respond for cocaine under extinction, while having no effect on instrumental responding for heroin or food.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSION</b>
</p>
<p>The present findings suggest masitinib, a drug with proven efficacy in CNS disorders, could represent a novel treatment for cocaine addiction provided its influence on the reinforcing and incentive properties of the drug is confirmed.</p>
</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" IndexingMethod="Curated" Owner="NLM"><PMID Version="1">29520592</PMID>
<DateCompleted><Year>2019</Year>
<Month>02</Month>
<Day>20</Day>
</DateCompleted>
<DateRevised><Year>2021</Year>
<Month>01</Month>
<Day>09</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1432-2072</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>235</Volume>
<Issue>5</Issue>
<PubDate><Year>2018</Year>
<Month>05</Month>
</PubDate>
</JournalIssue>
<Title>Psychopharmacology</Title>
<ISOAbbreviation>Psychopharmacology (Berl)</ISOAbbreviation>
</Journal>
<ArticleTitle>Decrease of cocaine, but not heroin, self-administration and relapse by the tyrosine kinase inhibitor masitinib in male Sprague Dawley rats.</ArticleTitle>
<Pagination><MedlinePgn>1545-1556</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1007/s00213-018-4865-0</ELocationID>
<Abstract><AbstractText Label="RATIONALE">Accumulating evidence shows that cocaine, and also heroin, influence several tyrosine kinases, expressed in neurons and in non-neuronal populations such as microglia, astrocytes and mast-cells. Drug-induced activation of mast cells both triggers inflammatory processes in the brain mediated by the glial cells they activate, and facilitates histamine release which may directly influence the dopamine system. Thus, by triggering the activation and degranulation of mast cells dependent on the tyrosine kinase c-kit and Fyn, the latter being also involved in NMDA-dependent synaptic plasticity, cocaine and heroin may indirectly influence the neural mechanisms that mediate their reinforcing properties. Masitinib, a novel tyrosine kinase inhibitor with high selectivity for c-Kit, Fyn and Lyn, may alter the aberrant consequences of the activation of these tyrosine kinases by cocaine and heroin.</AbstractText>
<AbstractText Label="OBJECTIVE">We investigated in rats the effect of a chronic oral treatment with masitinib (20 mg/kg) on the reinforcing and motivational properties of self-administered cocaine (250 μg/infusion) and heroin (40 μg/infusion).</AbstractText>
<AbstractText Label="METHODS">Three different cohorts of rats were trained instrumentally to respond for cocaine, heroin or food under continuous reinforcement. In each group, we assessed the influence of chronic daily treatment with masitinib on the maintenance of instrumental responding and intake and the motivation for the reinforcer. Thus, masitinib and vehicle-treated rats were challenged to adapt to high behavioural demand, to respond under a progressive ratio schedule of reinforcement and to reinstate instrumental responding after extinction and/or abstinence.</AbstractText>
<AbstractText Label="RESULTS">Masitinib selectively decreased cocaine intake, the motivation for cocaine and the subsequent propensity to respond for cocaine under extinction, while having no effect on instrumental responding for heroin or food.</AbstractText>
<AbstractText Label="CONCLUSION">The present findings suggest masitinib, a drug with proven efficacy in CNS disorders, could represent a novel treatment for cocaine addiction provided its influence on the reinforcing and incentive properties of the drug is confirmed.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Belin-Rauscent</LastName>
<ForeName>A</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Psychology, University of Cambridge, Downing Street, Cambridge, CB2 3EB, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Behavioural and Clinical Neuroscience Institute, University of Cambridge, Downing Street, Cambridge, CB2 3EB, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lacoste</LastName>
<ForeName>J</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Psychiatry & Addictology, CHU de Martinique, Fort de France, Martinique, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hermine</LastName>
<ForeName>O</ForeName>
<Initials>O</Initials>
<AffiliationInfo><Affiliation>AB Science, Paris, SA, France.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Institut Imagine INSERM U1163 and CNRS ERL8654, Centre de Reference des Mastocytoses, University of Paris Descartes, Paris, France.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Hematology, APHP, Necker Children's Hospital, Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Moussy</LastName>
<ForeName>A</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>AB Science, Paris, SA, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Everitt</LastName>
<ForeName>B J</ForeName>
<Initials>BJ</Initials>
<AffiliationInfo><Affiliation>Department of Psychology, University of Cambridge, Downing Street, Cambridge, CB2 3EB, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Behavioural and Clinical Neuroscience Institute, University of Cambridge, Downing Street, Cambridge, CB2 3EB, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Belin</LastName>
<ForeName>David</ForeName>
<Initials>D</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0002-7383-372X</Identifier>
<AffiliationInfo><Affiliation>Department of Psychology, University of Cambridge, Downing Street, Cambridge, CB2 3EB, UK. bdb26@cam.ac.uk.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Behavioural and Clinical Neuroscience Institute, University of Cambridge, Downing Street, Cambridge, CB2 3EB, UK. bdb26@cam.ac.uk.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>MR/N02530X/1</GrantID>
<Acronym>MRC_</Acronym>
<Agency>Medical Research Council</Agency>
<Country>United Kingdom</Country>
</Grant>
<Grant><GrantID>RG82507</GrantID>
<Acronym>MRC_</Acronym>
<Agency>Medical Research Council</Agency>
<Country>United Kingdom</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>03</Month>
<Day>08</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Germany</Country>
<MedlineTA>Psychopharmacology (Berl)</MedlineTA>
<NlmUniqueID>7608025</NlmUniqueID>
<ISSNLinking>0033-3158</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000701">Analgesics, Opioid</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D018765">Dopamine Uptake Inhibitors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D047428">Protein Kinase Inhibitors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D013844">Thiazoles</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>70D95007SX</RegistryNumber>
<NameOfSubstance UI="D003932">Heroin</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>I5Y540LHVR</RegistryNumber>
<NameOfSubstance UI="D003042">Cocaine</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>M59NC4E26P</RegistryNumber>
<NameOfSubstance UI="C526575">masitinib</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000284" MajorTopicYN="N">Administration, Oral</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000701" MajorTopicYN="N">Analgesics, Opioid</DescriptorName>
<QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016739" MajorTopicYN="N">Behavior, Addictive</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003042" MajorTopicYN="N">Cocaine</DescriptorName>
<QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003216" MajorTopicYN="N">Conditioning, Operant</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018765" MajorTopicYN="N">Dopamine Uptake Inhibitors</DescriptorName>
<QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003932" MajorTopicYN="N">Heroin</DescriptorName>
<QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009042" MajorTopicYN="N">Motivation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D047428" MajorTopicYN="N">Protein Kinase Inhibitors</DescriptorName>
<QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012008" MajorTopicYN="N">Recurrence</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012054" MajorTopicYN="N">Reinforcement, Psychology</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012646" MajorTopicYN="N">Self Administration</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013844" MajorTopicYN="N">Thiazoles</DescriptorName>
<QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Addiction</Keyword>
<Keyword MajorTopicYN="Y">Cocaine</Keyword>
<Keyword MajorTopicYN="Y">Heroin</Keyword>
<Keyword MajorTopicYN="Y">Mast cells</Keyword>
<Keyword MajorTopicYN="Y">Tyrosine kinase inhibitor</Keyword>
</KeywordList>
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<Month>07</Month>
<Day>12</Day>
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<Month>02</Month>
<Day>20</Day>
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Decrease of cocaine, but not heroin, self-administration and relapse by the tyrosine kinase inhibitor masitinib in male Sprague Dawley rats.

Decrease of cocaine, but not heroin, self-administration and relapse by the tyrosine kinase inhibitor masitinib in male Sprague Dawley rats.

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