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dc.contributor.author
Elmer, G. I.
dc.contributor.author
Pieper, J. O.
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Levy, J.
dc.contributor.author
Rubinstein, Marcelo
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dc.contributor.author
Low, Malcolm J.
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dc.contributor.author
Grandy, David K.
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dc.contributor.author
Wise, R.A.
dc.date.available
2019-07-19T16:22:12Z
dc.date.issued
2005-10
dc.identifier.citation
Elmer, G. I.; Pieper, J. O.; Levy, J.; Rubinstein, Marcelo; Low, Malcolm J.; et al.; Brain stimulation and morphine reward deficits in dopamine D2 receptor-deficient mice; Springer; Psychopharmacology; 182; 1; 10-2005; 33-44
dc.identifier.issn
0033-3158
dc.identifier.uri
http://hdl.handle.net/11336/79901
dc.description.abstract
Rationale: The rewarding effects of lateral hypothalamic brain stimulation, various natural rewards, and several drugs of abuse are attenuated by D1 or D2 dopamine receptor (D1R or D2R) antagonists. Much of the evidence for dopaminergic involvement in rewards is based on pharmacological agents with limited or "relative" selectivity for dopamine receptor subtypes. Genetically engineered animal models provide a complementary approach to pharmacological investigations. Objectives: In the present study, we explored the contribution of dopamine D2Rs to (1) brain stimulation reward (BSR) and (2) the potentiation of this behavior by morphine and amphetamine using D2R-deficient mice. Methods: Wild-type (D2Rwt), heterozygous (D2Rhet), and D2R knockout (D2Rko) mice were trained to turn a wheel for rewarding brain stimulation. Once equivalent rate-frequency curves were established, morphine-induced (0, 1.0, 3.0, and 5.6 mg/kg s.c.) and amphetamine-induced (0, 1.0, 2.0, and 4.0 mg/kg i.p.) potentiations of BSR were determined. Results: The D2Rko mice required approximately 50% more stimulation than the D2Rwt mice did. With the equi-rewarding levels of stimulation current, amphetamine potentiated BSR equally across the three genotypes. In contrast, morphine potentiated rewarding stimulation in the D2Rwt, had no effect in the D2Rhet, and antagonized rewarding stimulation in the D2Rko mice. Conclusions: D2R elimination decreases, but does not eliminate, the rewarding effects of lateral hypothalamic stimulation. After compensation for this deficit, amphetamine continues to potentiate BSR, while morphine does not.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Springer
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Addiction
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Amphetamine
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Depolarization
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Icss
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Knockout
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Mice
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Neuroleptic
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Opioid
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Reinforcement
dc.subject.classification
Neurociencias
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dc.subject.classification
Medicina Básica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Brain stimulation and morphine reward deficits in dopamine D2 receptor-deficient mice
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2019-07-18T13:01:03Z
dc.journal.volume
182
dc.journal.number
1
dc.journal.pagination
33-44
dc.journal.pais
Alemania
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dc.journal.ciudad
Berlin
dc.description.fil
Fil: Elmer, G. I.. University of Maryland; Estados Unidos
dc.description.fil
Fil: Pieper, J. O.. Behavioral Neuroscienc; Estados Unidos
dc.description.fil
Fil: Levy, J.. Behavioral Neuroscienc; Estados Unidos
dc.description.fil
Fil: Rubinstein, Marcelo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
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Fil: Low, Malcolm J.. Oregon Health and Science University; Estados Unidos
dc.description.fil
Fil: Grandy, David K.. Oregon Health and Science University; Estados Unidos
dc.description.fil
Fil: Wise, R.A.. Behavioral Neuroscienc; Estados Unidos
dc.journal.title
Psychopharmacology
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pubmed/16136297
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1007/s00213-005-0051-2
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/link.springer.com/article/10.1007/s00213-005-0051-2
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