Daily cocaine treatment produces a persistent reduction of [3H]dopamine uptake in vitro in rat nucleus accumbens but not in striatum

Izenwasser, Sari; Cox, Brian M.

doi:10.1016/0006-8993(90)90797-f

Cited by 100 publications

(38 citation statements)

References 10 publications

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“…Data from studies of DAT mRNA expression during and after exposure to cocaine are consistent with the results that showed downregulated dopamine uptake and inhibitor binding (120,121). Xia et al (122) have reported that DAT mRNA levels decreased 4 hr after the last injection of a chronic regimen of cocaine administration but not at 72 hr.…”

Section: Permeation Pathwaysupporting

confidence: 77%

Cellular and Molecular Aspects of Monoamine Neurotransmitter Transporters

Kitayama

Dohi

1996

Japanese Journal of Pharmacology

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Section: Permeation Pathwaysupporting

confidence: 77%

Cellular and Molecular Aspects of Monoamine Neurotransmitter Transporters

Kitayama

Dohi

1996

Japanese Journal of Pharmacology

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“…Such alterations in DA release may be the product of long-term adaptations in the mesolimbic DA system caused by repeated cocaine intake (Addy et al, 2010;Cass et al, 1993;Chen et al, 2008;Izenwasser and Cox, 1990;Kalivas and Duffy, 1990;Pettit et al, 1990). That said, drugassociated situational cues are known to alter DA system activity (Duvauchelle et al, 2000;Weitemier and Murphy, 2009) and expression of voluntary reward-seeking actions (Ostlund et al, 2010;Xie et al, 2012), and this raises the possibility that cocaine-induced learning contributed to the effects described here.…”

Section: Discussionmentioning

confidence: 86%

Phasic Mesolimbic Dopamine Signaling Encodes the Facilitation of Incentive Motivation Produced by Repeated Cocaine Exposure

Ostlund

LeBlanc

Kosheleff

et al. 2014

Neuropsychopharmacol

119

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Drug addiction is marked by pathological drug seeking and intense drug craving, particularly in response to drug-related stimuli. Repeated psychostimulant administration is known to induce long-term alterations in mesolimbic dopamine (DA) signaling that are hypothesized to mediate this heightened sensitivity to environmental stimuli. However, there is little direct evidence that drug-induced alteration in mesolimbic DA function underlies this hypersensitivity to motivational cues. In the current study, we tested this hypothesis using fast-scan cyclic voltammetry to monitor phasic DA signaling in the nucleus accumbens core of cocaine-pretreated (6 once-daily injections of 15 mg/kg, i.p.) and drug-naive rats during a test of cue-evoked incentive motivation for food-the Pavlovian-to-instrumental transfer task. We found that prior cocaine exposure augmented both reward seeking and DA release triggered by the presentation of a reward-paired cue. Furthermore, cue-evoked DA signaling positively correlated with cue-evoked food seeking and was found to be a statistical mediator of this behavioral effect of cocaine. Taken together, these findings provide support for the hypothesis that repeated cocaine exposure enhances cue-evoked incentive motivation through augmented phasic mesolimbic DA signaling. This work sheds new light on a fundamental neurobiological mechanism underlying motivated behavior and its role in the expression of compulsive reward seeking.

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“…This finding raises the question of the functional significance of DA co-released with noradrenaline. Moreover, a cocaineinsensitive DA transporter has been observed in rat brain (Izenwasser and Cox 1990;Elsworth et al 1993) and suggested in mouse brain (Moron et al 2002). In the frontal cortex, the number of DAT binding sites has been measured, and the ratio of low-to high-affinity binding sites was found to be significantly higher there than in the CPu or NAc (Boja et al 1990;Boja et al 1995).…”

Section: Discussionmentioning

confidence: 99%

Selective modifications in the nucleus accumbens of dopamine synaptic transmission in rats exposed to chronic stress

Scheggi

Leggio

Masi

et al. 2002

Journal of Neurochemistry

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Stressful events are accompanied by modifications in dopaminergic transmission in distinct brain regions. As the activity of the neuronal dopamine (DA) transporter (DAT) is considered to be a critical mechanism for determining the extent of DA receptor activation, we investigated whether a 3-week exposure to unavoidable stress, which produces a reduction in DA output in the nucleus accumbens shell (NAcS) and medial prefrontal cortex (mPFC), would affect DAT density and DA D 1 receptor complex activity in the NAcS, mPFC and caudate-putamen (CPu). Rats exposed to unavoidable stress showed a decreased DA output in the NAcS accompanied by a decrease in the number of DAT binding sites, and an increase in the number of DA D 1 binding sites and Vmax of SKF 38393-stimulated adenylyl cyclase. In the mPFC, stress exposure produced a decrease in DA output with no modification in DAT binding or in DA D 1 receptor complex activity. Moreover, in the CPu stress exposure induced no changes in DA output or in the other neurochemical variables examined. This study shows that exposure to a chronic unavoidable stress that produces a decrease in DA output in frontomesolimbic areas induced several adaptive neurochemical modifications selectively in the nucleus accumbens.

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Daily cocaine treatment produces a persistent reduction of [3H]dopamine uptake in vitro in rat nucleus accumbens but not in striatum

Cited by 100 publications

References 10 publications

Cellular and Molecular Aspects of Monoamine Neurotransmitter Transporters

Cellular and Molecular Aspects of Monoamine Neurotransmitter Transporters

Phasic Mesolimbic Dopamine Signaling Encodes the Facilitation of Incentive Motivation Produced by Repeated Cocaine Exposure

Selective modifications in the nucleus accumbens of dopamine synaptic transmission in rats exposed to chronic stress

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