Nicotine-conditioned single-trial place preference: selective role of nucleus accumbens shell dopamine D1 receptors in acquisition

Spina, Liliana; Fenu, Sandro; Longoni, R; Rivas, Emilia; Chiara, G. Di

doi:10.1007/s00213-005-0211-4

Cited by 87 publications

(68 citation statements)

References 48 publications

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“…Results from this study showed that nicotine given acutely in a previously drug naive animal elicited a DA-mediated aversion in a place conditioning paradigm, whereas other groups have shown DA-dependent acute nicotine reward (Acquas et al, 1989;Lecca et al, 2006;Merlo Pich et al, 1999;Pak et al, 2006;Sellings et al, 2008;Spina et al, 2006). Acute nicotine administered directly into the brain produces both rewarding and aversive effects (Laviolette et al, 2002;Sellings et al, 2008) that can be segregated within the nucleus accumbens (Sellings et al, 2008).…”

Section: Discussionmentioning

confidence: 78%

“…Nicotine also produces motivational effects through non-dopaminergic neural systems, such as the cholinergic tegmental pedunculopontine (TPP) nucleus (Lanca et al, 2000;Laviolette et al, 2002;Picciotto and Corrigall, 2002). The mesolimbic DA system has been implicated in the processing of the acute motivational properties of nicotine (Laviolette and van der Kooy, 2003;Laviolette et al, 2008;Spina et al, 2006;Tanabe et al, 2008); however, the involvement of dopaminergic signaling in the aversive response to chronic nicotine withdrawal is largely unknown.…”

Section: Introductionmentioning

confidence: 99%

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Dopaminergic Signaling Mediates the Motivational Response Underlying the Opponent Process to Chronic but Not Acute Nicotine

Grieder

Sellings

Vargas‐Perez

et al. 2009

Neuropsychopharmacol

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The mesolimbic dopamine (DA) system is implicated in the processing of the positive reinforcing effect of all drugs of abuse, including nicotine. It has been suggested that the dopaminergic system is also involved in the aversive motivational response to drug withdrawal, particularly for opiates, however, the role for dopaminergic signaling in the processing of the negative motivational properties of nicotine withdrawal is largely unknown. We hypothesized that signaling at dopaminergic receptors mediates chronic nicotine withdrawal aversions and that dopaminergic signaling would differentially mediate acute vs dependent nicotine motivation. We report that nicotine-dependent rats and mice showed conditioned place aversions to an environment paired with abstinence from chronic nicotine that were blocked by the DA receptor antagonist a-flupenthixol (a-flu) and in DA D 2 receptor knockout mice. Conversely, a-flu pretreatment had no effect on preferences for an environment paired with abstinence from acute nicotine. Taken together, these results suggest that dopaminergic signaling is necessary for the opponent motivational response to nicotine in dependent, but not non-dependent, rodents. Further, signaling at the DA D 2 receptor is critical in mediating withdrawal aversions in nicotine-dependent animals. We suggest that the alleviation of nicotine withdrawal primarily may be driving nicotine motivation in dependent animals. Neuropsychopharmacology (2010) 35, 943-954;

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Section: Discussionmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Dopaminergic Signaling Mediates the Motivational Response Underlying the Opponent Process to Chronic but Not Acute Nicotine

Grieder

Sellings

Vargas‐Perez

et al. 2009

Neuropsychopharmacol

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“…In addition, rats learn to lever-press for administration of cocaine or amphetamine into the ventromedial striatum (Ikemoto, 2003;Ikemoto et al, 2005), and various other drugs into medial A10 Zangen et al, 2002Zangen et al, , 2006Rodd et al, 2004;Ikemoto et al, 2006). Further, blockade of dopamine receptors or lesions of dopaminergic terminals in the ventromedial striatum, but not the ventrolateral striatum, disrupts the establishment of conditioned place preference induced by systemic administration of cocaine, amphetamine, nicotine, or morphine (Sellings and Clarke, 2003;Fenu et al, 2006;Sellings et al, 2006a, b;Spina et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Dual Role of Medial A10 Dopamine Neurons in Affective Encoding

Shin

Ikemoto

2008

Neuropsychopharmacol

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Increasing evidence suggests that the activation of medial A10 neurons mediates positive affective encoding. However, little is known about the functions of the inhibition of midbrain dopamine neurons. Here we show evidence suggesting that the inhibition of medial A10 neurons mediates a negative affective state, leading to negative affective encoding, whereas blunting the activation of medial A10 neurons disrupts positive affective encoding involving food reward. We used a microinjection procedure, in which the D 2 dopamine receptor agonist quinpirole was administered into the cell body region of the dopamine neurons, a procedure that reduces dopamine cell firing. Microinjections of quinpirole into the posteromedial ventral tegmental area, but not its more lateral counterparts, led to conditioned place aversion. Quinpirole administration to this site also decreased food intake and basal dopamine concentration in the ventromedial striatum, a major projection area of medial A10 neurons. In addition, moderate quinpirole doses that did not lead to conditioned place aversion or disrupt food intake abolished food-conditioned place preference, suggesting that blunting dopamine impulse activity in response to food reward disrupts positive affective encoding in associated external stimuli. Our data support the hypothesis that activation of medial A10 dopamine neurons mediates a positive affective state, leading to positive affective encoding, while their inhibition mediates a negative affective state, leading to negative affective encoding. Together with previous findings, we propose that medial A10 neurons are an important component of the mechanism via which animals learn to avoid negative incentive stimuli.

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“…A number of studies have demonstrated that nonspecific or dopamine D 1 -specific receptor antagonists can interfere with both appetitive and aversive conditioning induced by both drug and non-drug reinforcers (Azzara et al, 2001;Beninger and Miller, 1998;Dalley et al, 2005;Di Chiara, 2002;Eyny and Horvitz, 2003;Fenu and Di Chiara, 2003;Greba et al, 2001;Greba and Kokkinidis, 2000;Hiroi and White, 1991;Hunt et al, 1985;Inoue et al, 2000;Nader and LeDoux, 1999;Pruitt et al, 1995;Smith-Roe and Kelley, 2000), and several of these also found that dopamine D 2 receptor blockade did not prevent acquisition of conditioning ( Caulliez et al, 1996;Cervo and Samanin, 1995;Fenu et al, 2001;Shippenberg and Heidbreder, 1995;Spina et al, 2006).…”

Section: Acquisition Of Conditioned Suppressionmentioning

confidence: 99%

“…Using a wide variety of procedures, previous studies have shown that dopamine D 1 and/or D 2 receptor antagonists can interfere with the expression of conditioned drug effects (Adams et al, 2001;Baker et al, 2003;Cervo and Samanin, 1996;de Oliveira et al, 2006;Fontana et al, 1993;Guarraci et al, 1999;Hiroi and White, 1991;Inoue et al, 2000;Schenk and Gittings, 2003;Spina et al, 2006;Weissenborn et al, 1996). However, there has been little consistency across these studies in whether dopamine D 1 or D 2 receptor antagonists are more effective in blocking this expression.…”

Section: Expression Of Conditioned Suppressionmentioning

confidence: 99%

Differential involvement of dopamine receptors in conditioned suppression induced by cocaine

Grakalic

Panlilio

Thorndike

et al. 2007

European Journal of Pharmacology

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Cocaine-paired stimuli can suppress food-reinforced operant behavior in rats, providing an animal model of conditioned drug effects. To study the neuropharmacological basis of this phenomenon, we examined the effects of various dopamine receptor antagonists on the acquisition and expression of cocaine-induced conditioned suppression in rats. Superimposed on an ongoing baseline of foodreinforced operant responding, a stimulus was paired with response-independent cocaine (3.0 mg/ kg, i.v.) during each of 8 training sessions. To study acquisition, independent groups of rats were given saline, the dopamine D 1 -like receptor antagonist R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride (SCH23390) (0.001-0.03 mg/kg, i.p.), or the dopamine D 2 -like receptor antagonist eticlopride (0.001-0.03 mg/kg, i.p.) prior to each training session. To study expression, independent groups of rats were trained first, then given saline, SCH23390, eticlopride, or N-[4-(4-(2-methoxyphenyl)piperazinyl)butyl]-2-naphthamide (BP897) (a dopamine D 3 partial receptor agonist; 0.1-1.0 mg/kg, i.p.) before test sessions in which the stimulus was presented without cocaine. Pretreatment with either SCH23390 or eticlopride during acquisition reduced the direct suppressant effects of cocaine, but conditioning was blocked only in rats that were treated with SCH23390 during acquisition training. Expression of conditioning was attenuated only by eticlopride. Thus, dopamine at least partially mediates both the acquisition and expression of cocaine-induced conditioned suppression, with activation of dopamine D 1 -and D 2 -like receptors underlying these respective processes.

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Nicotine-conditioned single-trial place preference: selective role of nucleus accumbens shell dopamine D1 receptors in acquisition

Abstract: The results indicate that dopamine D1 but not D2 receptors of the NAc shell are specifically involved in the acquisition of nicotine-induced CPP.

Cited by 87 publications

References 48 publications

Dopaminergic Signaling Mediates the Motivational Response Underlying the Opponent Process to Chronic but Not Acute Nicotine

Dopaminergic Signaling Mediates the Motivational Response Underlying the Opponent Process to Chronic but Not Acute Nicotine

Dual Role of Medial A10 Dopamine Neurons in Affective Encoding

Differential involvement of dopamine receptors in conditioned suppression induced by cocaine

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