Anterior ventral tegmental area dopaminergic neurons are not involved in the motivational effects of bromocriptine, pramipexole and cocaine in drug-free rats.
Identifieur interne : 000583 ( PubMed/Corpus ); précédent : 000582; suivant : 000584Anterior ventral tegmental area dopaminergic neurons are not involved in the motivational effects of bromocriptine, pramipexole and cocaine in drug-free rats.
Auteurs : Omar Ouachikh ; Wisam Dieb ; Franck Durif ; Aziz HafidiSource :
- Behavioural brain research [ 1872-7549 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Benzothiazoles (pharmacology), Bromocriptine (pharmacology), Cocaine (pharmacology), Conditioning (Psychology) (drug effects), Dopamine Agonists (pharmacology), Dopaminergic Neurons (drug effects), Male, Motivation (drug effects), Motivation (physiology), Motor Activity (drug effects), Rats, Rats, Sprague-Dawley, Ventral Tegmental Area (drug effects), Ventral Tegmental Area (physiology).
- MESH :
- chemical , pharmacology : Benzothiazoles, Bromocriptine, Cocaine, Dopamine Agonists.
- drug effects : Conditioning (Psychology), Dopaminergic Neurons, Motivation, Motor Activity, Ventral Tegmental Area.
- physiology : Motivation, Ventral Tegmental Area.
- Animals, Male, Rats, Rats, Sprague-Dawley.
Abstract
Dopamine dysregulation syndrome in Parkinson's disease has been attributed to dopamine replacement therapies and/or a lesion of the dopaminergic system. Dopaminergic neuronal loss targets the substantia nigra and the ventral tegmental area (VTA). We hypothesize that dopamine replacement therapy is responsible for the potential reinforcement effect in Parkinson's disease, by acting on the neuronal reward circuitry. We previously demonstrated that the posterior (p) VTA, which projects to the nucleus accumbens (NAc), is implicated in the motivational effect of dopamine receptor agonists in 6-OHDA bilateral pVTA-lesioned drug-free animals. In the present study we investigated the implication of the anterior (a) VTA in the potential reinforcement effect of dopamine receptor agonists. Using the conditioned place preference (CPP) behavioral paradigm, we investigated the motivational effects of dopamine receptor agonists (bromocriptine and pramipexole), and cocaine in rats with a 6-OHDA bilateral lesion of the aVTA. Bromocriptine and pramipexole did not induce a significant CPP at 1mg/kg in both sham and bilateral 6-OHDA-lesioned rats. However bromocriptine induced CPP only at a dose of 3mg/kg in both animal groups. Moreover cocaine, which is known to increase dopamine release, induced reinforcing effects in both 6-OHDA-lesioned and sham rats. Our data show a lack of involvement of aVTA dopamine neurons in the motivational effects of bromocriptine, pramipexole and cocaine.
DOI: 10.1016/j.bbr.2013.12.021
PubMed: 24361908
Links to Exploration step
pubmed:24361908Le document en format XML
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Electronic address: azhafidi@univ-bpclermont.fr.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Behavioural brain research</title><idno type="eISSN">1872-7549</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Benzothiazoles (pharmacology)</term><term>Bromocriptine (pharmacology)</term><term>Cocaine (pharmacology)</term><term>Conditioning (Psychology) (drug effects)</term><term>Dopamine Agonists (pharmacology)</term><term>Dopaminergic Neurons (drug effects)</term><term>Male</term><term>Motivation (drug effects)</term><term>Motivation (physiology)</term><term>Motor Activity (drug effects)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Ventral Tegmental Area (drug effects)</term><term>Ventral Tegmental Area (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Benzothiazoles</term><term>Bromocriptine</term><term>Cocaine</term><term>Dopamine Agonists</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Conditioning (Psychology)</term><term>Dopaminergic Neurons</term><term>Motivation</term><term>Motor Activity</term><term>Ventral Tegmental Area</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Motivation</term><term>Ventral Tegmental Area</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Male</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dopamine dysregulation syndrome in Parkinson's disease has been attributed to dopamine replacement therapies and/or a lesion of the dopaminergic system. Dopaminergic neuronal loss targets the substantia nigra and the ventral tegmental area (VTA). We hypothesize that dopamine replacement therapy is responsible for the potential reinforcement effect in Parkinson's disease, by acting on the neuronal reward circuitry. We previously demonstrated that the posterior (p) VTA, which projects to the nucleus accumbens (NAc), is implicated in the motivational effect of dopamine receptor agonists in 6-OHDA bilateral pVTA-lesioned drug-free animals. In the present study we investigated the implication of the anterior (a) VTA in the potential reinforcement effect of dopamine receptor agonists. Using the conditioned place preference (CPP) behavioral paradigm, we investigated the motivational effects of dopamine receptor agonists (bromocriptine and pramipexole), and cocaine in rats with a 6-OHDA bilateral lesion of the aVTA. Bromocriptine and pramipexole did not induce a significant CPP at 1mg/kg in both sham and bilateral 6-OHDA-lesioned rats. However bromocriptine induced CPP only at a dose of 3mg/kg in both animal groups. Moreover cocaine, which is known to increase dopamine release, induced reinforcing effects in both 6-OHDA-lesioned and sham rats. Our data show a lack of involvement of aVTA dopamine neurons in the motivational effects of bromocriptine, pramipexole and cocaine.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24361908</PMID><DateCreated><Year>2014</Year><Month>02</Month><Day>17</Day></DateCreated><DateCompleted><Year>2014</Year><Month>10</Month><Day>14</Day></DateCompleted><DateRevised><Year>2014</Year><Month>02</Month><Day>17</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-7549</ISSN><JournalIssue CitedMedium="Internet"><Volume>262</Volume><PubDate><Year>2014</Year><Month>Apr</Month><Day>01</Day></PubDate></JournalIssue><Title>Behavioural brain research</Title><ISOAbbreviation>Behav. Brain Res.</ISOAbbreviation></Journal><ArticleTitle>Anterior ventral tegmental area dopaminergic neurons are not involved in the motivational effects of bromocriptine, pramipexole and cocaine in drug-free rats.</ArticleTitle><Pagination><MedlinePgn>1-7</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbr.2013.12.021</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0166-4328(13)00764-X</ELocationID><Abstract><AbstractText>Dopamine dysregulation syndrome in Parkinson's disease has been attributed to dopamine replacement therapies and/or a lesion of the dopaminergic system. Dopaminergic neuronal loss targets the substantia nigra and the ventral tegmental area (VTA). We hypothesize that dopamine replacement therapy is responsible for the potential reinforcement effect in Parkinson's disease, by acting on the neuronal reward circuitry. We previously demonstrated that the posterior (p) VTA, which projects to the nucleus accumbens (NAc), is implicated in the motivational effect of dopamine receptor agonists in 6-OHDA bilateral pVTA-lesioned drug-free animals. In the present study we investigated the implication of the anterior (a) VTA in the potential reinforcement effect of dopamine receptor agonists. Using the conditioned place preference (CPP) behavioral paradigm, we investigated the motivational effects of dopamine receptor agonists (bromocriptine and pramipexole), and cocaine in rats with a 6-OHDA bilateral lesion of the aVTA. Bromocriptine and pramipexole did not induce a significant CPP at 1mg/kg in both sham and bilateral 6-OHDA-lesioned rats. However bromocriptine induced CPP only at a dose of 3mg/kg in both animal groups. Moreover cocaine, which is known to increase dopamine release, induced reinforcing effects in both 6-OHDA-lesioned and sham rats. Our data show a lack of involvement of aVTA dopamine neurons in the motivational effects of bromocriptine, pramipexole and cocaine.</AbstractText><CopyrightInformation>Copyright © 2013 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ouachikh</LastName><ForeName>Omar</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Clermont Université, Université d'Auvergne, EA7280, Laboratoire de Neuropsychopharmacologie des systèmes dopaminergiques sous corticaux, Clermont-Ferrand, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dieb</LastName><ForeName>Wisam</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Clermont Université, Université d'Auvergne, EA7280, Laboratoire de Neuropsychopharmacologie des systèmes dopaminergiques sous corticaux, Clermont-Ferrand, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Durif</LastName><ForeName>Franck</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Clermont Université, Université d'Auvergne, EA7280, Laboratoire de Neuropsychopharmacologie des systèmes dopaminergiques sous corticaux, Clermont-Ferrand, France; CHU Clermont-Ferrand, Service de Neurologie, 63000 Clermont-Ferrand, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hafidi</LastName><ForeName>Aziz</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Clermont Université, Université d'Auvergne, EA7280, Laboratoire de Neuropsychopharmacologie des systèmes dopaminergiques sous corticaux, Clermont-Ferrand, France. Electronic address: azhafidi@univ-bpclermont.fr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>12</Month><Day>19</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Behav Brain Res</MedlineTA><NlmUniqueID>8004872</NlmUniqueID><ISSNLinking>0166-4328</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D052160">Benzothiazoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018491">Dopamine Agonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>3A64E3G5ZO</RegistryNumber><NameOfSubstance UI="D001971">Bromocriptine</NameOfSubstance></Chemical><Chemical><RegistryNumber>83619PEU5T</RegistryNumber><NameOfSubstance UI="C061333">pramipexole</NameOfSubstance></Chemical><Chemical><RegistryNumber>I5Y540LHVR</RegistryNumber><NameOfSubstance UI="D003042">Cocaine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D052160" MajorTopicYN="N">Benzothiazoles</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001971" MajorTopicYN="N">Bromocriptine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003042" MajorTopicYN="N">Cocaine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003213" MajorTopicYN="N">Conditioning (Psychology)</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018491" MajorTopicYN="N">Dopamine Agonists</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059290" MajorTopicYN="N">Dopaminergic Neurons</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009042" MajorTopicYN="N">Motivation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009043" MajorTopicYN="N">Motor Activity</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</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="D017557" MajorTopicYN="N">Ventral Tegmental Area</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">6-OHDA</Keyword><Keyword MajorTopicYN="N">Conditioned place preference</Keyword><Keyword MajorTopicYN="N">Parkinson</Keyword><Keyword MajorTopicYN="N">Reward</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>10</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2013</Year><Month>12</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>12</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>12</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>12</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>10</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24361908</ArticleId><ArticleId IdType="pii">S0166-4328(13)00764-X</ArticleId><ArticleId IdType="doi">10.1016/j.bbr.2013.12.021</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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