Effects of opioid and dopamine receptor antagonists on relapse induced by stress and re-exposure to heroin in rats.
Identifieur interne : 001F82 ( Main/Corpus ); précédent : 001F81; suivant : 001F83Effects of opioid and dopamine receptor antagonists on relapse induced by stress and re-exposure to heroin in rats.
Auteurs : Y. Shaham ; J. StewartSource :
- Psychopharmacology [ 0033-3158 ] ; 1996.
English descriptors
- KwdEn :
- Animals (MeSH), Behavior, Animal (drug effects), Dopamine (metabolism), Dopamine Antagonists (pharmacology), Heroin (pharmacology), Male (MeSH), Microdialysis (MeSH), Motor Activity (drug effects), Naltrexone (pharmacology), Narcotic Antagonists (MeSH), Narcotics (pharmacology), Nucleus Accumbens (metabolism), Raclopride (MeSH), Rats (MeSH), Salicylamides (pharmacology), Self Administration (MeSH), Stress, Physiological (MeSH).
- MESH :
- chemical , metabolism : Dopamine.
- drug effects : Behavior, Animal, Motor Activity.
- metabolism : Nucleus Accumbens.
- chemical , pharmacology : Dopamine Antagonists, Heroin, Naltrexone, Narcotics, Salicylamides.
- Animals, Male, Microdialysis, Narcotic Antagonists, Raclopride, Rats, Self Administration, Stress, Physiological.
Abstract
The effects of blockade of opioid and dopamine receptors on relapse to heroin-seeking induced by footshock stress and re-exposure to heroin were examined in a reinstatement procedure. Male rats were trained to self-administer heroin (100 micrograms/kg per infusion, IV; four 3-h sessions/day for 8-11 consecutive days). Extinction sessions were given for 5-7 days during which saline was substituted for heroin. In nine groups, the effects on relapse induced by footshock (10 min, 0.5 mA, 0.5 s on with a mean off period of 40 s), heroin priming (0.25 mg/kg), and saline priming were studied after pretreatment with either naltrexone (1 or 10 mg/kg, SC), the D1-like receptor antagonist SCH 23390 (0.05 or 0.1 mg/kg, IP), the D2-like receptor antagonist raclopride (0.25 or 0.5 mg/kg, IP), the mixed dopamine antagonist flupenthixol decanoate (3 or 6 mg/kg, IM), or IP injection of saline (control condition). Naltrexone, flupenthixol, raclopride, and the highest dose of SCH 23,390 attenuated heroin-induced relapse: only the mixed DA receptor antagonist, flupenthixol, attenuated foot-shock-induced relapse. These results, and those from microdialysis showing that heroin elicits greater locomotor activity and DA release in the nucleus accumbens than footshock, suggest that the neurochemical events underlying stress- and heroin-induced relapse are not identical.
DOI: 10.1007/BF02246022
PubMed: 8826544
Links to Exploration step
pubmed:8826544Le document en format XML
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Stewart</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1996">1996</date><idno type="RBID">pubmed:8826544</idno><idno type="pmid">8826544</idno><idno type="doi">10.1007/BF02246022</idno><idno type="wicri:Area/Main/Corpus">001F82</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">001F82</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Effects of opioid and dopamine receptor antagonists on relapse induced by stress and re-exposure to heroin in rats.</title><author><name sortKey="Shaham, Y" sort="Shaham, Y" uniqKey="Shaham Y" first="Y" last="Shaham">Y. Shaham</name><affiliation><nlm:affiliation>Department of Psychology, Concordia University, Montreal, Quebec, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Stewart, J" sort="Stewart, J" uniqKey="Stewart J" first="J" last="Stewart">J. Stewart</name></author></analytic><series><title level="j">Psychopharmacology</title><idno type="ISSN">0033-3158</idno><imprint><date when="1996" type="published">1996</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Behavior, Animal (drug effects)</term><term>Dopamine (metabolism)</term><term>Dopamine Antagonists (pharmacology)</term><term>Heroin (pharmacology)</term><term>Male (MeSH)</term><term>Microdialysis (MeSH)</term><term>Motor Activity (drug effects)</term><term>Naltrexone (pharmacology)</term><term>Narcotic Antagonists (MeSH)</term><term>Narcotics (pharmacology)</term><term>Nucleus Accumbens (metabolism)</term><term>Raclopride (MeSH)</term><term>Rats (MeSH)</term><term>Salicylamides (pharmacology)</term><term>Self Administration (MeSH)</term><term>Stress, Physiological (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Behavior, Animal</term><term>Motor Activity</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Nucleus Accumbens</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Dopamine Antagonists</term><term>Heroin</term><term>Naltrexone</term><term>Narcotics</term><term>Salicylamides</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Male</term><term>Microdialysis</term><term>Narcotic Antagonists</term><term>Raclopride</term><term>Rats</term><term>Self Administration</term><term>Stress, Physiological</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The effects of blockade of opioid and dopamine receptors on relapse to heroin-seeking induced by footshock stress and re-exposure to heroin were examined in a reinstatement procedure. Male rats were trained to self-administer heroin (100 micrograms/kg per infusion, IV; four 3-h sessions/day for 8-11 consecutive days). Extinction sessions were given for 5-7 days during which saline was substituted for heroin. In nine groups, the effects on relapse induced by footshock (10 min, 0.5 mA, 0.5 s on with a mean off period of 40 s), heroin priming (0.25 mg/kg), and saline priming were studied after pretreatment with either naltrexone (1 or 10 mg/kg, SC), the D1-like receptor antagonist SCH 23390 (0.05 or 0.1 mg/kg, IP), the D2-like receptor antagonist raclopride (0.25 or 0.5 mg/kg, IP), the mixed dopamine antagonist flupenthixol decanoate (3 or 6 mg/kg, IM), or IP injection of saline (control condition). Naltrexone, flupenthixol, raclopride, and the highest dose of SCH 23,390 attenuated heroin-induced relapse: only the mixed DA receptor antagonist, flupenthixol, attenuated foot-shock-induced relapse. These results, and those from microdialysis showing that heroin elicits greater locomotor activity and DA release in the nucleus accumbens than footshock, suggest that the neurochemical events underlying stress- and heroin-induced relapse are not identical.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8826544</PMID><DateCompleted><Year>1996</Year><Month>12</Month><Day>06</Day></DateCompleted><DateRevised><Year>2019</Year><Month>07</Month><Day>26</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0033-3158</ISSN><JournalIssue CitedMedium="Print"><Volume>125</Volume><Issue>4</Issue><PubDate><Year>1996</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Psychopharmacology</Title><ISOAbbreviation>Psychopharmacology (Berl)</ISOAbbreviation></Journal><ArticleTitle>Effects of opioid and dopamine receptor antagonists on relapse induced by stress and re-exposure to heroin in rats.</ArticleTitle><Pagination><MedlinePgn>385-91</MedlinePgn></Pagination><Abstract><AbstractText>The effects of blockade of opioid and dopamine receptors on relapse to heroin-seeking induced by footshock stress and re-exposure to heroin were examined in a reinstatement procedure. Male rats were trained to self-administer heroin (100 micrograms/kg per infusion, IV; four 3-h sessions/day for 8-11 consecutive days). Extinction sessions were given for 5-7 days during which saline was substituted for heroin. In nine groups, the effects on relapse induced by footshock (10 min, 0.5 mA, 0.5 s on with a mean off period of 40 s), heroin priming (0.25 mg/kg), and saline priming were studied after pretreatment with either naltrexone (1 or 10 mg/kg, SC), the D1-like receptor antagonist SCH 23390 (0.05 or 0.1 mg/kg, IP), the D2-like receptor antagonist raclopride (0.25 or 0.5 mg/kg, IP), the mixed dopamine antagonist flupenthixol decanoate (3 or 6 mg/kg, IM), or IP injection of saline (control condition). Naltrexone, flupenthixol, raclopride, and the highest dose of SCH 23,390 attenuated heroin-induced relapse: only the mixed DA receptor antagonist, flupenthixol, attenuated foot-shock-induced relapse. These results, and those from microdialysis showing that heroin elicits greater locomotor activity and DA release in the nucleus accumbens than footshock, suggest that the neurochemical events underlying stress- and heroin-induced relapse are not identical.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shaham</LastName><ForeName>Y</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Psychology, Concordia University, Montreal, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stewart</LastName><ForeName>J</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. 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