Voluntary Nicotine Consumption Triggers<i>In Vivo</i>Potentiation of Cortical Excitatory Drives to Midbrain Dopaminergic Neurons

Caillé, Stéphanie; Guillem, Karine; Cador, Martine; Manzoni, Olivier J.; Georges, François

doi:10.1523/jneurosci.2950-09.2009

Cited by 37 publications

(33 citation statements)

References 26 publications

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“…PPAR a receptors can exert tonic inhibition of DA cell activity, as their antagonism increases the spontaneous firing rate of VTA DA neurons (Melis et al, 2010). Accordingly, deficient OEA tone may contribute to enhanced spontaneous firing and burst activity of VTA DA cells that is more pronounced following a history of nicotine SA vs YA (Caille et al, 2009). The PPAR a influence on VTA DA cell activity likely occurs through a negative modulation of a 4 b 2 -nACh receptor expression or function (Melis et al, 2010), and it is conceivable that reduced PPAR a activation resulting from deficient OEA tone contributes to enhanced VTA a 4 b 2 -nACh receptor expression that is more pronounced following nicotine SA vs YA (Metaxas et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…The volitional nature of nicotine exposure may also influence the neurochemical stimuli that provoke AEA production. For example, nicotine SA and YA produce distinct alterations in nAChR expression, DA D 2 receptor binding, and corticosterone levels (Caille et al, 2009;Donny et al, 2000;Metaxas et al, 2010), and each of these systems can influence the production of AEA and related ethanolamides (Centonze et al, 2004;Di et al, 2003Di et al, , 2005Giuffrida et al, 1999;Hill et al, 2010a, b;Stella and Piomelli, 2001). …”

Section: Endocannabinoid Levels Following Nicotine Exposure Mw Buczynmentioning

confidence: 99%

“…As indexed by VTA microdialysis, nicotine SA induced greater decrements in baseline OEA levels and greater drug-induced increases in AEA levels than did forced YA. Each of these effects may contribute to enhanced activity and excitability of VTA DA neurons evident following chronic self-administered, but not forced, nicotine exposure (Caille et al, 2009;Metaxas et al, 2010), an effect that likely enhances both the direct and conditioned reinforcing effects of the drug. The present data also demonstrate that nicotine-induced increases in VTA 2-AG levels are influenced by drug history, but not by response contingency.…”

Section: The Volitional Nature Of Nicotine Exposure Also Influences Bmentioning

confidence: 99%

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The Volitional Nature of Nicotine Exposure Alters Anandamide and Oleoylethanolamide Levels in the Ventral Tegmental Area

Buczynski

Polis

Parsons

2012

Neuropsychopharmacol

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Cannabinoid-1 receptors (CB 1 ) have an important role in nicotine reward and their function is disrupted by chronic nicotine exposure, suggesting nicotine-induced alterations in endocannabinoid (eCB) signaling. However, the effects of nicotine on brain eCB levels have not been rigorously evaluated. Volitional intake of nicotine produces physiological and behavioral effects distinct from forced drug administration, although the mechanisms underlying these effects are not known. This study compared the effects of volitional nicotine self-administration (SA) and forced nicotine exposure (yoked administration (YA)) on levels of eCBs and related neuroactive lipids in the ventral tegmental area (VTA) and other brain regions. Brain lipid levels were indexed both by in vivo microdialysis in the VTA and lipid extractions from brain tissues. Nicotine SA, but not YA, reduced baseline VTA dialysate oleoylethanolamide (OEA) levels relative to nicotine-naïve controls, and increased anandamide (AEA) release during nicotine intake. In contrast, all nicotine exposure paradigms increased VTA dialysate 2-arachidonoyl glycerol (2-AG) levels. Thus, nicotine differentially modulates brain lipid (2-AG, AEA, and OEA) signaling, and these modulations are influenced by the volitional nature of the drug exposure. Corresponding bulk tissue analysis failed to identify these lipid changes. Nicotine exposure had no effect on fatty acid amide hydrolase activity in the VTA, suggesting that changes in AEA and OEA signaling result from alterations in their nicotine-induced biosynthesis. Both CB 1 (by AEA and 2-AG) and non-CB 1 (by OEA) targets can alter the excitability and activity of the dopaminergic neurons in the VTA. Collectively, these findings implicate disrupted lipid signaling in the motivational effects of nicotine.

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Section: Discussionmentioning

confidence: 99%

Section: Endocannabinoid Levels Following Nicotine Exposure Mw Buczynmentioning

confidence: 99%

Section: The Volitional Nature Of Nicotine Exposure Also Influences Bmentioning

confidence: 99%

See 1 more Smart Citation

The Volitional Nature of Nicotine Exposure Alters Anandamide and Oleoylethanolamide Levels in the Ventral Tegmental Area

Buczynski

Polis

Parsons

2012

Neuropsychopharmacol

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“…Neuroadaptations that are caused by repeated passive exposure to the drug itself have been widely studied (Nestler, 1992;Lüscher and Malenka, 2011), but there are further changes in brain function that reflect the memory of drug experience. These further brain changes are seen in animals that self-administer the drug, but are absent in animals that have passively received 'yoked' injections of the same drug at the same dose and temporal pattern (Wang et al, 2005;You et al, 2007You et al, , 2008Chen et al, 2008;Caillé et al, 2009). Here, we were concerned with brain changes involved in the consolidation of the memory for drug-environment association established by Pavlovian conditioning.…”

Section: Introductionmentioning

confidence: 99%

Dopamine in the Dorsal Hippocampus Impairs the Late Consolidation of Cocaine-Associated Memory

Kramar

Chefer

Wise

et al. 2014

Neuropsychopharmacol

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Cocaine is thought to be addictive because it elevates dopamine levels in the striatum, reinforcing drug-seeking habits. Cocaine also elevates dopamine levels in the hippocampus, a structure involved in contextual conditioning as well as in reward function. Hippocampal dopamine promotes the late phase of consolidation of an aversive step-down avoidance memory. Here, we examined the role of hippocampal dopamine function in the persistence of the conditioned increase in preference for a cocaine-associated compartment. Blocking dorsal hippocampal D1-type receptors (D1Rs) but not D2-type receptors (D2Rs) 12 h after a single training trial extended persistence of the normally short-lived memory; conversely, a general and a specific phospholipase C-coupled D1R agonist (but not a D2R or adenylyl cyclase-coupled D1R agonist) decreased the persistence of the normally long-lived memory established by three-trial training. These effects of D1 agents were opposite to those previously established in a step-down avoidance task, and were here also found to be opposite to those in a lithium chloride-conditioned avoidance task. After returning to normal following cocaine injection, dopamine levels in the dorsal hippocampus were found elevated again at the time when dopamine antagonists and agonists were effective: between 13 and 17 h after cocaine injection. These findings confirm that, long after the making of a cocaine-place association, hippocampal activity modulates memory consolidation for that association via a dopaminedependent mechanism. They suggest a dynamic role for dorsal hippocampal dopamine in this late-phase memory consolidation and, unexpectedly, differential roles for late consolidation of memories for places that induce approach or withdrawal because of a drug association.

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“…Chronic and voluntary intake of drugs of abuse in animals has different neurological consequences than passive intake of the same substances or intake of natural rewards, such as sucrose (Dumont et al, 2005;Martin et al, 2006;Chen et al, 2008;You et al, 2008;Caillé et al, 2009;Kalant, 2010). For example, rats with a history of cocaine or nicotine self-administration demonstrate enhanced (in magnitude or duration) AMPA-mediated responses in several areas of the brain reward system, but these changes are not seen in rats self-administering a natural reward or when drug intake is passive (Dumont et al, 2005;Martin et al, 2006;Chen et al, 2008;You et al, 2008;Caillé et al, 2009;Kalant, 2010).…”

Section: Introductionmentioning

confidence: 99%

A Switch in the Neuromodulatory Effects of Dopamine in the Oval Bed Nucleus of the Stria Terminalis Associated with Cocaine Self-Administration in Rats

Krawczyk¹,

Sharma²,

Mason³

et al. 2011

Journal of Neuroscience

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Chronic exposure to drugs of abuse alters brain reward circuits and produces functional changes in the dopamine (DA) system. However, it is not known whether these changes are directly related to drug-driven behaviors or whether they simply are adaptive responses to long-term drug exposure. Here, we combined the rat model of cocaine self-administration with brain slice electrophysiology to identify drug-use related alterations in the neuromodulatory effects of DA in the oval bed nucleus of the stria terminalis (ovBST), a robust DA terminal field. Long-Evans rats self-administered cocaine intravenously (0.75 mg/kg/injection) for an average of 15 d, on reward-lean or -rich schedules of reinforcement. Brain slice recordings conducted 20 h after the last self-administration session revealed a reversal of the neuromodulatory effect of DA on GABA A -IPSCs. Specifically, the effect of DA switched from a D2-mediated decrease in drug-naive rats to a D1-receptor-mediated increase in GABA A -IPSC in cocaine self-administering rats. Furthermore, the switch in DA modulation of GABA A -IPSC remained after a 30 d withdrawal period. In contrast, this switch was not observed after the acquisition phase of cocaine self-administration, when rats received cocaine passively, or in rats maintaining sucrose self-administration. Therefore, our study reveals a reversal in the effects of DA on inhibitory transmission, from reduction to enhancement, in the ovBST of cocaine selfadministering rats. This change was unique to voluntary intake of cocaine and maintained after a withdrawal period, suggesting a mechanism underlying the maintenance of cocaine self-administration and perhaps craving during drug-free periods.

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Voluntary Nicotine Consumption TriggersIn VivoPotentiation of Cortical Excitatory Drives to Midbrain Dopaminergic Neurons

Cited by 37 publications

References 26 publications

The Volitional Nature of Nicotine Exposure Alters Anandamide and Oleoylethanolamide Levels in the Ventral Tegmental Area

The Volitional Nature of Nicotine Exposure Alters Anandamide and Oleoylethanolamide Levels in the Ventral Tegmental Area

Dopamine in the Dorsal Hippocampus Impairs the Late Consolidation of Cocaine-Associated Memory

A Switch in the Neuromodulatory Effects of Dopamine in the Oval Bed Nucleus of the Stria Terminalis Associated with Cocaine Self-Administration in Rats

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