Previous Exposure to Psychostimulants Enhances the Reinstatement of Cocaine Seeking by Nucleus Accumbens AMPA

Suto, Nobuyoshi; Tanabe, Lauren M.; Austin, Jotham R.; Creekmore, Elizabeth; Pham, Chauchau T; Vezina, Paul

doi:10.1038/sj.npp.1300533

Cited by 103 publications

(110 citation statements)

References 62 publications

(96 reference statements)

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“…Cocaine-induced reinstatement is dependent on increased glutamatergic signaling within the prefrontal cortex or nucleus accumbens (Cornish and Kalivas, 2000;Capriles et al, 2003;McFarland et al, 2003;Baptista et al, 2004;Di Ciano and Everitt, 2004;Suto et al, 2004). In the present study, N-acetylcysteine administered before daily cocaine prevents the establishment of plasticity needed for cocaine-induced reinstatement because behavior is measured 2-3 weeks after the last N-acetylcysteine treatment.…”

Section: Discussionmentioning

confidence: 95%

“…However, this may reflect the existence of multiple, functionally distinct pools of glutamate. Cocaine increases glutamate in the synaptic cleft after corticostriatal activation, thereby generating behaviors dependent on postsynaptic receptor stimulation (Cornish and Kalivas, 2000;McFarland et al, 2003;Di Ciano and Everitt, 2004;Suto et al, 2004). Conversely, N-acetylcysteine involves glutamate release into the extrasynaptic compartment resulting in the stimulation of group II mGluRs (Baker et al, 2002(Baker et al, , 2003Moran et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

RepeatedN-Acetylcysteine Administration Alters Plasticity-Dependent Effects of Cocaine

Madayag¹,

Lobner²,

Kau³

et al. 2007

J. Neurosci.

206

242

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Cocaine produces a persistent reduction in cystine-glutamate exchange via system x c Ϫ in the nucleus accumbens that may contribute to pathological glutamate signaling linked to addiction. System x c Ϫ influences glutamate neurotransmission by maintaining basal, extracellular glutamate in the nucleus accumbens, which, in turn, shapes synaptic activity by stimulating group II metabotropic glutamate autoreceptors. In the present study, we tested the hypothesis that a long-term reduction in system x c Ϫ activity is part of the plasticity produced by repeated cocaine that results in the establishment of compulsive drug seeking. To test this, the cysteine prodrug N-acetylcysteine was administered before daily cocaine to determine the impact of increased cystine-glutamate exchange on the development of plasticity-dependent cocaine seeking. Although N-acetylcysteine administered before cocaine did not alter the acute effects of cocaine on self-administration or locomotor activity, it prevented behaviors produced by repeated cocaine including escalation of drug intake, behavioral sensitization, and cocaine-primed reinstatement. Because sensitization or reinstatement was not evident even 2-3 weeks after the last injection of N-acetylcysteine, we examined whether N-acetylcysteine administered before daily cocaine also prevented the persistent reduction in system x c Ϫ activity produced by repeated cocaine. Interestingly, N-acetylcysteine pretreatment prevented cocaine-induced changes in [35 S]cystine transport via system x c Ϫ, basal glutamate, and cocaine-evoked glutamate in the nucleus accumbens when assessed at least 3 weeks after the last N-acetylcysteine pretreatment. These findings indicate that N-acetylcysteine selectively alters plasticity-dependent behaviors and that normal system x c Ϫ activity prevents pathological changes in extracellular glutamate that may be necessary for compulsive drug seeking.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

RepeatedN-Acetylcysteine Administration Alters Plasticity-Dependent Effects of Cocaine

Madayag¹,

Lobner²,

Kau³

et al. 2007

J. Neurosci.

206

242

View full text Add to dashboard Cite

show abstract

“…Infusions of an mGluR 2/3 agonist into the NAc decrease glutamate release . Intra-NAc injections of an AMPA receptor antagonist attenuate reinstatement of cocaine priming-induced reinstatement of drug seeking, (Cornish and Kalivas, 2000) while intra-NAc AMPA injections reinstate cocaine seeking (Cornish and Kalivas, 2000;Suto et al, 2004). There is also evidence that glutamate transmission in the NAc is involved in conditioned drug effects.…”

Section: Introductionmentioning

confidence: 99%

Activation of Group II Metabotropic Glutamate Receptors in the Nucleus Accumbens Shell Attenuates Context-Induced Relapse to Heroin Seeking

Bossert

Gray

Lü

et al. 2005

Neuropsychopharmacol

215

173

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Using a rat relapse model, we previously reported that re-exposing rats to a drug-associated context, following extinction of operant responding in a different context, reinstates heroin seeking. In an initial pharmacological characterization, we found that the mGluR 2/3 agonist LY379268, which acts centrally to reduce evoked glutamate release, attenuates context-induced reinstatement of heroin seeking when injected systemically or into the ventral tegmental area, the cell body region of the mesolimbic dopamine system. Here, we tested whether injections of LY379268 into the nucleus accumbens (NAc), a terminal region of the mesolimbic dopamine system, would also attenuate context-induced reinstatement of heroin seeking. Rats were trained to self-administer heroin; drug infusions were paired with a discrete tone-light cue. Subsequently, lever pressing was extinguished in the presence of the discrete cue in a context that differed from the drug self-administration context in terms of visual, auditory, tactile, and circadian cues. After extinction of responding, LY379268 was injected to different groups of rats into the NAc core or shell or into the caudate-putamen, a terminal region of the nigrastriatal dopamine system. Injections of LY379268 into the NAc shell (0.3 or 1.0 mg) dose-dependently attenuated context-induced reinstatement of heroin seeking. Injections of 1.0 mg of LY379268 into the NAc core had no effect, while a higher dose (3.0 mg) decreased this reinstatement. Injections of LY379268 (3.0 mg) 1.5 mm dorsal from the NAc core into the caudate-putamen were ineffective. Results suggest an important role of glutamate transmission in the NAc shell in context-induced reinstatement of heroin seeking.

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“…There are two major classes of ionotropic glutamate receptors: AMPA/kainate and NMDA. While AMPA receptors in the nucleus accumbens are critically involved in the reinstatement of cocaine-seeking behavior [9,10,30,32,40], there is evidence that NMDA receptors may also play a role. For example, systemic administration of MK-801, an NMDA receptor channel blocker, robustly reinstated cocaine seeking, without an increase in nonspecific operant responding [12, but see also 6].…”

mentioning

confidence: 99%

When administered into the nucleus accumbens core or shell, the NMDA receptor antagonist AP-5 reinstates cocaine-seeking behavior in the rat

Famous

Schmidt

Pierce

2007

Neuroscience Letters

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Cocaine craving in human addicts can be elicited by three major factors: environmental cues associated with drug taking, a stressful life-event or re-exposure to cocaine [26]. Drug craving is modeled in rodents and non-human primates using the reinstatement model of cocaine seeking [13,19,39]. The nucleus accumbens plays a major role in mediating the reinstatement of cocaine seeking [27,36]. The nucleus accumbens receives a major dopaminergic projection from the ventral tegmental area (VTA) and glutamatergic projections from the prefrontal cortex, hippocampus and amygdala [5,34,43]. The accumbens is composed of two major subregions, the core and the shell, which have differential afferent and efferent anatomical projections [7,20,21,44]. Functionally, the accumbens shell is considered the more limbic subregion, mediating the acute effects of drug reward [8,35]. In contrast, the core is more involved in the compulsivity of drug addiction [16] and the effects of drug-associated cues [14,18,25]. In terms of cocaine priming-induced reinstatement of drug seeking, dopamine receptors play differential roles in the shell versus the core [2][3][4]. For example, infusion of dopamine receptor antagonists into the accumbens shell, but not the core, attenuates the reinstatement of cocaine-seeking behavior [2][3][4]. Similarly, dopamine receptor agonists promote the reinstatement of cocaine seeking when microinjected into the shell, but not core [4,37]. Collectively, these studies demonstrate that increased dopamine transmission in the nucleus accumbens shell, but not the core, critically mediates the reinstatement of cocaineseeking behavior.The glutamatergic projection from the medial prefrontal cortex (mPFC) to the nucleus accumbens is one of the key anatomical substrates underlying cocaine priming-induced reinstatement of drug seeking [27,37]. There are two major classes of ionotropic glutamate receptors: AMPA/kainate and NMDA. While AMPA receptors in the nucleus accumbens are critically involved in the reinstatement of cocaine-seeking behavior [9,10,30,32,40], there is evidence that NMDA receptors may also play a role. For example, systemic administration of MK-801, an NMDA receptor channel blocker, robustly reinstated cocaine seeking, without an increase in nonspecific operant responding [12, but see also 6]. In a subsequent study, it was found that intra-accumbal administration of the competitive NMDA receptor antagonist, CPP, had no effect on the reinstatement of cocaine seeking when administered either alone or prior Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. to a systemic...

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Previous Exposure to Psychostimulants Enhances the Reinstatement of Cocaine Seeking by Nucleus Accumbens AMPA

Cited by 103 publications

References 62 publications

RepeatedN-Acetylcysteine Administration Alters Plasticity-Dependent Effects of Cocaine

RepeatedN-Acetylcysteine Administration Alters Plasticity-Dependent Effects of Cocaine

Activation of Group II Metabotropic Glutamate Receptors in the Nucleus Accumbens Shell Attenuates Context-Induced Relapse to Heroin Seeking

When administered into the nucleus accumbens core or shell, the NMDA receptor antagonist AP-5 reinstates cocaine-seeking behavior in the rat

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