Dissociation Between the Time Course of Ethanol and Extracellular Dopamine Concentrations in the Nucleus Accumbens After a Single Intraperitoneal Injection

Yim, Hyeon Joo; Robinson, Donita L.; White, Martha L.; Jaworski, Jason N.; Randall, Patrick K.; Lancaster, Francine E.; Gonzales, Rueben A.

doi:10.1111/j.1530-0277.2000.tb02056.x

Cited by 54 publications

(41 citation statements)

References 30 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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“…injections of drugs such as ethanol also produce substantial, albeit transient, increases in DA release. However, accumbal DA concentrations rapidly return to basal levels despite the continued presence of elevated brain concentrations of ethanol (Yim et al, 2000). A similar cell body-terminal relation may explain in part why primates will self-administer single 15 s 'pulses' of toluene (3000 ppm) (Weiss et al, 1979), but changes in accumbal DA release in rats are not apparent during continuous exposure to the same concentration of solvent (Gerasimov et al, 2002).…”

Section: -Ohda Studies and Toluenementioning

confidence: 96%

Toluene-Induced Locomotor Activity is Blocked by 6-Hydroxydopamine Lesions of the Nucleus Accumbens and the mGluR2/3 Agonist LY379268

Riegel

Ali

French

2003

Neuropsychopharmacol

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The abuse of volatile inhalants remains a prominent, yet poorly understood, form of substance abuse among youth. Nevertheless, the identification of a mechanism underlying the reinforcing properties of inhalants has been hampered by the lack of a clearly identifiable neural substrate upon which these chemicals act. One ingredient that is common to many abused inhalants is toluene, an organic solvent that is self-administered by nonhuman primates and rodents. Most drugs of abuse have been found to elicit forward locomotion in rats, an effect owing to the activation of mesoaccumbal dopamine (DA) pathways. Thus, the present study was undertaken using two different approaches to determine whether toluene-induced locomotor hyperactivity is also ultimately dependent upon DA neurotransmission in the mesolimbic nucleus accumbens (NAC). Here we report on the effects of 6-hydroxydopamine (6-OHDA) lesions of the NAC or pretreatment with the metabotropic mGlu2/3 receptor agonist LY379268 on toluene-induced locomotor activity. Both procedures, which are known to alter neurotransmission within the NAC, significantly attenuated toluene's locomotor stimulatory effects. These results provide strong support for a central mechanism of action of inhalants, which in the past has been more typically attributed to general nonspecific mechanisms throughout the brain. Moreover, as with other drugs of abuse, the NAC may be the final common pathway subserving toluene's abuse liability.

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“…Previous studies clearly demonstrate that intra-accumbal dopamine and ethanol time courses dissociate rapidly following i.p. or oral ethanol administration (Yim et al, 2000;Doyon et al, 2005). Therefore, it appears likely that other mechanisms, in addition to the κ-opioid system, regulate ethanol-induced dopamine activity.…”

Section: Discussionmentioning

confidence: 99%

κ-Opioid receptor modulation of accumbal dopamine concentration during operant ethanol self-administration

et al. 2006

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Our study examined ethanol self-administration and accumbal dopamine concentration during κ-opioid receptor (KOPr) blockade. Long-Evans rats were trained to respond for 20 min of access to 10% ethanol (with sucrose) over 7 days. Rats were injected s.c. with the long-acting KOPr antagonist, nor-binaltorphimine (NOR-BNI; 0 or 20 mg/kg) 15-20 h prior to testing. Microdialysis revealed a transient elevation in dopamine concentration within 5 min of ethanol access in controls. NOR-BNItreated rats did not exhibit this response, but showed a latent increase in dopamine concentration at the end of the access period. The rise in dopamine levels correlated positively with dialysate ethanol concentration but not in controls. NOR-BNI did not alter dopamine levels in rats self-administering 10% sucrose. The transient dopamine response during ethanol acquisition in controls is consistent with previous results that were attributed to ethanol stimulus cues. The altered dopamine response to NOR-BNI during ethanol drinking suggests that KOPr blockade temporarily uncovered a pharmacological stimulation of dopamine release by ethanol. Despite these neurochemical changes, NOR-BNI did not alter operant responding or ethanol intake, suggesting that the KOPr is not involved in ethanol-reinforced behavior under the limited conditions we studied.

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Dissociation Between the Time Course of Ethanol and Extracellular Dopamine Concentrations in the Nucleus Accumbens After a Single Intraperitoneal Injection

Cited by 54 publications

References 30 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

Toluene-Induced Locomotor Activity is Blocked by 6-Hydroxydopamine Lesions of the Nucleus Accumbens and the mGluR2/3 Agonist LY379268

κ-Opioid receptor modulation of accumbal dopamine concentration during operant ethanol self-administration

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