Dose-dependent effect of ethanol on extracellular dopamine in mesolimbic striatum of awake rhesus monkeys: comparison with cocaine across individuals

Bradberry, Charles W.

doi:10.1007/s00213-002-1233-9

Cited by 45 publications

(14 citation statements)

References 73 publications

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“…Our present work also parallels an emerging view that the NAc DA release observed following investigator-administered alcohol was provoked by novelty, unexpectedness, and/or aversiveness of the administration (Bradberry, 2002; Gonzales et al, 2004; Heidbreder and De Witte, 1993; Imperato and Di Chiara, 1986; Joseph et al, 2003; Marinelli et al, 2003; Philpot and Kirstein, 1998; Yan, 1999; Yim et al, 1998, 2000; Yoshimoto et al, 1992). Although several studies have documented increases in NAc [DA] during oral self-administration of alcohol (Doyon et al, 2005; Gonzales and Weiss, 1998; Melendez et al, 2002; Weiss et al, 1992, 1993, 1996), Doyon and colleagues (2003, 2005) showed that increases in NAc [DA] were dissociated from changes in brain ethanol concentration: NAc DA levels peaked 5 minutes after the onset of oral alcohol self-administration, then gradually tapered off over the next 30 minutes as the animals continued to drink alcohol and brain ethanol levels continued to rise.…”

Section: Discussionsupporting

confidence: 84%

When What You See Isn’t What You Get: Alcohol Cues, Alcohol Administration, Prediction Error, and Human Striatal Dopamine

Yoder

Morris

Constantinescu

et al. 2008

Alcoholism Clin & Exp Res

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Section: Discussionsupporting

confidence: 84%

When What You See Isn’t What You Get: Alcohol Cues, Alcohol Administration, Prediction Error, and Human Striatal Dopamine

Yoder

Morris

Constantinescu

et al. 2008

Alcoholism Clin & Exp Res

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“…Across species, EtOH shares with cocaine the ability to acutely increase brain DA concentrations (e.g., Bradberry, 2002; Di Chiara and Imperato, 1988; Yoder et al, 2009), which has long been identified as the primary mechanism of cocaine’s abuse-related effects (e.g., Koob and Volkow, 2010; Pierce and Kumaresan, 2006). Moreover, brain-imaging studies in both cocaine and alcohol abusers have indicated that chronic consumption results in decreased brain DA D2-like receptors (for review see Cosgrove 2010) and a hypofunctional state of DA neurotransmission (e.g., Henry et al, 2009; Karkhanis et al, 2015; Parsons et al, 1991; Weiss et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

“…Enhancement of cocaine’s abuse-related effects by EtOH would be expected based on its ability to increase striatal dopamine (DA) concentrations (e.g., Bradberry, 2002; Di Chiara and Imperato, 1988; Yoder et al, 2009). Moreover, similar alterations in brain DA systems—particularly D2 receptors—have been observed in alcoholics and cocaine abusers (e.g., Cosgrove, 2010; Volkow et al, 1996,1999, 2002).…”

Section: Introductionmentioning

confidence: 99%

Effects of chronic binge-like ethanol consumption on cocaine self-administration in rhesus monkeys

Czoty

2015

Drug and Alcohol Dependence

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Background Most cocaine abusers also abuse alcohol, but little is known about interactions that promote co-abuse. These experiments in rhesus monkeys determined the effects of >8 weeks of ethanol (EtOH) consumption on cocaine self-administration (n=6), effects of dopamine (DA) receptor antagonists on cocaine reinforcement (n=3–4 per drug) and the ability of the D2-like DA receptor agonist quinpirole to elicit yawning (n=3). Methods Monkeys self-administered cocaine (0.0–1.0 mg/kg/injection, i.v.) under a 300-second fixed-interval schedule and the above-listed variables were measured before EtOH exposure. Next, monkeys consumed a sweetened, 4% EtOH solution in the home cage under binge-like conditions: one hour, 5 days/week with daily intake equaling 2.0 g/kg EtOH. After approximately 8 weeks, measures were re-determined, then EtOH drinking was discontinued. Finally, acute effects of EtOH on cocaine self-administration were determined by infusing EtOH (0.0–1.0 g/kg. i.v.) prior to cocaine self-administration sessions (n=4). Results In 5 of 6 monkeys, EtOH drinking increased self-administration of low cocaine doses but did not alter reinforcing effects of higher doses. Self-administration returned to baseline after EtOH access was terminated (n=3). Effects of DA receptor antagonists on cocaine self-administration were not consistently altered after EtOH consumption, but the ability of quinpirole to induce yawning was enhanced in 2 of 3 monkeys. Acute EtOH infusions only decreased self-administration of lower cocaine doses. Conclusions Taken together, the data suggest that long-term EtOH exposure can increase sensitivity to cocaine, possibly by increasing D3 receptor sensitivity. Data do not support a role for acute pharmacological interactions in promoting cocaine/EtOH co-abuse.

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“…Microdialysis studies in the behaving animal demonstrated that response-independent, systemic administration of cocaine, amphetamine, heroin, cannabinoids, nicotine, and ethanol increase dopamine levels in the NAcc (DiChiara 1986; Imperato and Di Chiara 1986; Imperato et al 1986; Di Chiara and Imperato 1988; Kalivas and Duffy 1990; Kuczesnki et al 1991; Yoshimoto et al 1992; Pontieri et al 1996; Tanda et al 1997). The dose of the drug administered and the concentration of striatal dopamine following drug administration are positively correlated, as demonstrated for cocaine and ethanol (Nicolaysen et al 1988; Bradberry 2002). Similar to response-independent drug administration, self-administered drugs of abuse, including cocaine, amphetamine, heroin and ethanol, induce increases in concentrations of dopamine in the NAcc (Hurd et al 1989, 1990; Pettit and Justice 1989, 1991; Weiss et al 1992, 1993; Di Ciano et al 1995; Wise et al 1995a, b).…”

Section: Effects Of Drugs Of Abuse On Extracellular Dopamine Concenmentioning

confidence: 91%

Dopamine Signaling in the Nucleus Accumbens of Animals Self-Administering Drugs of Abuse

Willuhn

Wanat

Clark

et al. 2009

Current Topics in Behavioral Neurosciences

171

159

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Abuse of psychoactive substances can lead to drug addiction. In animals, addiction is best modeled by drug self-administration paradigms. It has been proposed that the crucial common denominator for the development of drug addiction is the ability of drugs of abuse to increase extracellular concentrations of dopamine in the nucleus accumbens (NAcc). Studies using in vivo microdialysis and chronoamperometry in the behaving animal have demonstrated that drugs of abuse increase tonic dopamine concentrations in the NAcc. However, it is known that dopamine neurons respond to reward-related stimuli on a subsecond timescale. Thus, it is necessary to collect neurochemical information with this level of temporal resolution, as achieved with in vivo fast-scan cyclic voltammetry (FSCV), to fully understand the role of phasic dopamine release in normal behavior and drug addiction. We review studies that investigated the effects of drugs of abuse on NAcc dopamine levels in freely-moving animals using in vivo microdialysis, chronoamperometry and FSCV. After a brief introduction of dopamine anatomy and signal transduction, and a section on current theories of dopamine in natural goal-directed behavior, a discussion of techniques for the in vivo assessment of extracellular dopamine behaving animals is presented. Then, we review studies using these techniques to investigate changes in phasic and tonic dopamine signaling in the NAcc during 1) response-dependent and –independent administration of abused drugs, 2) drug-conditioned stimuli and operant behavior in self-administration paradigms, 3) drug withdrawal, and 4) cue-induced reinstatement of drug seeking. These results are then integrated with current ideas on the role of dopamine in addiction with an emphasis on a model illustrating phasic and tonic NAcc dopamine signaling during different stages of drug addiction. This model predicts that phasic dopamine release in response to drug-related stimuli will be enhanced over stimuli associated with natural reinforcers, which may result in aberrant goal-directed behaviors contributing to drug addiction.

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Dose-dependent effect of ethanol on extracellular dopamine in mesolimbic striatum of awake rhesus monkeys: comparison with cocaine across individuals

Cited by 45 publications

References 73 publications

When What You See Isn’t What You Get: Alcohol Cues, Alcohol Administration, Prediction Error, and Human Striatal Dopamine

When What You See Isn’t What You Get: Alcohol Cues, Alcohol Administration, Prediction Error, and Human Striatal Dopamine

Effects of chronic binge-like ethanol consumption on cocaine self-administration in rhesus monkeys

Dopamine Signaling in the Nucleus Accumbens of Animals Self-Administering Drugs of Abuse

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