Leão, Rodrigo M. [UNESP]Cruz, Fábio C. [UNESP]Carneiro-De-Oliveira, Paulo E. [UNESP]Rossetto, Daniella B. [UNESP]Valentini, Sandro Roberto [UNESP]Zanelli, Cleslei Fernando [UNESP]Planeta, Cleopatra da Silva [UNESP]2014-05-272014-05-272013-03-01Pharmacology Biochemistry and Behavior, v. 104, n. 1, p. 169-176, 2013.0091-30571873-5177http://hdl.handle.net/11449/74684We investigated the behavioral and molecular interactions between cocaine and nicotine, through evaluating locomotor activity, nicotine intravenous self-administration and gene expression. Locomotor sensitization was induced in male Wistar rats by repeated cocaine (20 mg/kg; i.p.) or saline injections once a day over 7 days. Three days after the last injection, rats were challenged with either saline or cocaine (15 mg/kg; i.p.) and the locomotor activity was measured. The very next day animals received either saline or nicotine (0.4 mg/kg; s.c.) and the locomotor cross-sensitization was tested. Animals were then prepared with intrajugular catheters for nicotine self-administration. Nicotine self-administration patterns were evaluated using fixed or progressive ratio schedules of reinforcement and a 24-h unlimited access binge. Immediately after the binge sessions animals were decapitated, the brains were removed and the nucleus accumbens was dissected. The dynorphin (DYN), μ-opioid receptor (mu opioid), neuropeptide Y (NPY), brain-derived neurotrophic factor (BDNF), tropomyosin-related tyrosine kinase B receptor (TrkB) and corticotropin- releasing factor receptor type 1 (CRF-R1) gene expression were measured by the reverse transcription-polymerase chain reaction (RT-PCR). Pretreatment with cocaine caused sensitization of cocaine motor response and locomotor cross-sensitization with nicotine. In the self-administration experiments repeated cocaine administration caused an increase in the nicotine break point and nicotine intake during a 24 h binge session. © 2013 Elsevier Inc.169-176engBDNFCocaineGene expressionLocomotor activityNicotineRT-PCRSelf-administrationbrain derived neurotrophic factorbrain derived neurotrophic factor receptorcocainecorticotropin releasing factordynorphinmu opiate receptornicotinesodium chlorideanimal experimentanimal modelanimal tissuebrain tissuecontrolled studycross allergydecapitationdrug seeking behaviorgene expressionlocomotionmalenonhumannucleus accumbenspriority journalratreinforcementreverse transcription polymerase chain reactionAnimalsBrain-Derived Neurotrophic FactorDynorphinsGene ExpressionMaleMotor ActivityNeuropeptide YNucleus AccumbensRatsRats, WistarReceptor, trkBReceptors, Corticotropin-Releasing HormoneReceptors, Opioid, muRisk FactorsSelf AdministrationTobacco Use DisorderAnimaliaRattusRattus norvegicusArtigo10.1016/j.pbb.2013.01.007WOS:000316594400022Acesso aberto2-s2.0-848741551302-s2.0-84874155130.pdf5333250355049814251476254528094215256654089001950000-0002-1378-63270000-0001-7831-1149