Prefrontal/accumbal catecholamine system determines motivational salience attribution to both reward- and aversion-related stimuli

Ventura, Rossella; Morrone, Cristina; Puglisi-Allegra, Stefano

doi:10.1073/pnas.0610178104

Cited by 170 publications

(198 citation statements)

References 34 publications

(58 reference statements)

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“…However, depletions of NE can produce deficits in conditioned place preference and conditioned place aversion (Ventura et al, 2007), which is consistent with the hypothesis that decreases in NE activity disrupt contextual conditioning. Additionally, previous research has demonstrated that atomoxetine (a NE reuptake inhibitor) reversed nicotine withdrawalrelated deficits in contextual fear conditioning (Davis and Gould, 2007).…”

Section: Discussionsupporting

confidence: 86%

Bupropion dose-dependently reverses nicotine withdrawal deficits in contextual fear conditioning

Portugal

Gould

2007

Pharmacology Biochemistry and Behavior

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Bupropion, a norepinephrine and dopamine reuptake inhibitor and nicotinic acetylcholine receptor antagonist, facilitates smoking cessation and reduces some symptoms of nicotine withdrawal. However, the effects of bupropion on nicotine withdrawal-associated deficits in learning remain unclear. The present study investigated whether bupropion has effects on contextual and cued fear conditioning following withdrawal from chronic nicotine or when administered alone. Bupropion was administered alone for a range of doses (2.5, 5, 10, 20 or 40 mg/kg), and dose-dependent impairments in contextual and cued fear conditioning were observed (20 or 40 mg/kg). Follow-up studies investigated if bupropion disrupted acquisition or expression of fear conditioning. Bupropion (40 mg/kg) administration on training day only produced deficits in contextual fear conditioning. Alternatively, bupropion (20 or 40 mg/kg) administration during testing dose-dependently produced deficits in contextual and cued fear conditioning. To test the effect of bupropion on nicotine withdrawal, mice were withdrawn from 12 days of chronic nicotine (6.3 mg/kg/day) or saline treatment. Withdrawal from chronic nicotine disrupted contextual fear conditioning; however, 5 mg/ kg bupropion reversed this deficit. Overall, these results indicate that a low dose of bupropion can reverse nicotine withdrawal deficits in contextual fear conditioning, but that high doses of bupropion produce deficits in fear conditioning.

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Section: Discussionsupporting

confidence: 86%

Bupropion dose-dependently reverses nicotine withdrawal deficits in contextual fear conditioning

Portugal

Gould

2007

Pharmacology Biochemistry and Behavior

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“…It has been reported that NE and ␣ 2 -ARs play a role in both positive and negative valence-learned behaviors (Ventura et al 2007). However, most studies exploring extinction behavior have utilized negative valence-learned behaviors.…”

Section: Yohimbine Impairs Extinction Of Cocaine Cppmentioning

confidence: 99%

Yohimbine impairs extinction of cocaine-conditioned place preference in an α₂-adrenergic receptor independent process

Davis¹,

Shields²,

Brigman³

et al. 2008

Learn. Mem.

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Extinction, a form of learning that has the ability to reshape learned behavior based on new experiences, has been heavily studied utilizing fear learning paradigms. Mechanisms underlying extinction of positive-valence associations, such as drug self-administration and place preference, are poorly understood yet may have important relevance to addiction treatment. Data suggest a major role for the noradrenergic system in extinction of fear-based learning. Employing both pharmacological and genetic approaches, we investigated the role of the ␣ 2 -adrenergic receptor (␣ 2 -AR) in extinction of cocaine-conditioned place preference (CPP) and glutamatergic transmission in the bed nucleus of the stria terminalis (BNST). We found that pre-extinction systemic treatment with the ␣ 2 -AR antagonist yohimbine impaired cocaine CPP extinction in C57BL/6J mice, an effect that was not mimicked by the more selective ␣ 2 -AR antagonist, atipamezole. Moreover, ␣ 2A -AR knockout mice exhibited similar cocaine CPP extinction and exacerbated extinction impairing effects of yohimbine. Using acute brain slices and electrophysiological approaches, we found that yohimbine produces a slowly evolving depression of glutamatergic transmission in the BNST that was not mimicked by atipamezole. Further, this action was extant in slices from ␣ 2A -AR knockout mice. Our data strongly suggest that extinction-modifying effects of yohimbine are unlikely to be due to actions at ␣ 2A -ARs.

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“…Male mice of the inbred C57BL/6JIco strain (Charles River Laboratories, Wilmington, MA), 8-9-week-old at the time of the experiments, were housed as previously described (Ventura et al, 2007). All experiments were conducted in accordance with Italian national law (Decreto Legislativo no.…”

Section: Animalsmentioning

confidence: 99%

“…The coordinates were measured according to the atlas of (Franklin and Paxinos, 1997). Monoamine tissue level analysis were as described previously (Ventura et al, 2007).…”

Section: -Ht Depletion In the Mpfcmentioning

confidence: 99%

Prefrontal/Amygdalar System Determines Stress Coping Behavior Through 5-HT/GABA Connection

Andolina

Maran

Valzania

et al. 2013

Neuropsychopharmacol

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Coping is defined as the behavioral and physiological effort made to master stressful situations. The ability to cope with stress leads either to healthy or to pathogenic outcomes. The medial prefrontal cortex (mpFC) and amygdala are acknowledged as having a major role in stress-related behaviors, and mpFC has a critical role in the regulation of amygdala-mediated arousal in response to emotionally salient stimuli. Prefrontal cortical serotonin (5-hydroxytryptamine (5-HT)) is involved in corticolimbic circuitry, and GABA has a major role in amygdala functioning. Here, using mice, it was assessed whether amygdalar GABA regulation by prefrontal 5-HT is involved in processing stressful experiences and in determining coping outcomes. First (experiment 1), bilateral selective 5-HT depletion in mpFC of mice reduced GABA release induced by stress in basolateral amygdala (BLA) and passive coping in the Forced Swimming Test (FST) (experiment 2). Moreover, prefrontal-amygdala disconnection procedure that combined a selective unilateral 5-HT depletion of mpFC and infusion of an inhibitor of GABA synthesis into the contralateral BLA, thereby to disrupt prefrontal-amygdalar serial connectivity bilaterally, showed that disconnection selectively decreases immobility in the FST. These results point to prefrontal/amygdala connectivity mediated by 5-HT and GABA transmission as a critical neural mechanism in stress-induced behavior.

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Prefrontal/accumbal catecholamine system determines motivational salience attribution to both reward- and aversion-related stimuli

Cited by 170 publications

References 34 publications

Bupropion dose-dependently reverses nicotine withdrawal deficits in contextual fear conditioning

Bupropion dose-dependently reverses nicotine withdrawal deficits in contextual fear conditioning

Yohimbine impairs extinction of cocaine-conditioned place preference in an α₂-adrenergic receptor independent process

Prefrontal/Amygdalar System Determines Stress Coping Behavior Through 5-HT/GABA Connection

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Prefrontal/accumbal catecholamine system determines motivational salience attribution to both reward- and aversion-related stimuli

Cited by 170 publications

References 34 publications

Bupropion dose-dependently reverses nicotine withdrawal deficits in contextual fear conditioning

Bupropion dose-dependently reverses nicotine withdrawal deficits in contextual fear conditioning

Yohimbine impairs extinction of cocaine-conditioned place preference in an α2-adrenergic receptor independent process

Prefrontal/Amygdalar System Determines Stress Coping Behavior Through 5-HT/GABA Connection

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Yohimbine impairs extinction of cocaine-conditioned place preference in an α₂-adrenergic receptor independent process