Dopamine in the prefrontal cortex regulates rats behavioral flexibility to changing reward value

Winter, Sabrina; Dieckmann, Marco; Schwabe, Kerstin

doi:10.1016/j.bbr.2008.10.040

Cited by 49 publications

(39 citation statements)

References 51 publications

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“…The ventral tegmental area (VTA) sends dopaminergic projections to the OFC (Berger et al, 1991;Dunnett and Robbins, 1992;Frankle et al, 2006;Geisler et al, 2007;Sesack and Grace, 2010). Furthermore, dopaminergic neurotransmission in the frontal cortices critically regulates higher-order cognitive function, including reward-related processing by the OFC that likely facilitates cocaine-seeking behavior (Cetin et al, 2004;Dalley et al, 2004;Kheramin et al, 2004;Ragozzino et al, 1999;Ward et al, 2009;Winter et al, 2009). Systemic dopamine D1-like receptor antagonism impairs drug context-induced cocaine-seeking behavior (Crombag et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Contribution of a Mesocorticolimbic Subcircuit to Drug Context-Induced Reinstatement of Cocaine-Seeking Behavior in Rats

Lasseter

Xie

Arguello

et al. 2013

Neuropsychopharmacol

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Cocaine-seeking behavior triggered by drug-paired environmental context exposure is dependent on orbitofrontal cortex (OFC)-basolateral amygdala (BLA) interactions. Here, we present evidence supporting the hypothesis that dopaminergic input from the ventral tegmental area (VTA) to the OFC critically regulates these interactions. In experiment 1, we employed site-specific pharmacological manipulations to show that dopamine D1-like receptor stimulation in the OFC is required for drug context-induced reinstatement of cocaine-seeking behavior following extinction training in an alternate context. Intra-OFC pretreatment with the dopamine D1-like receptor antagonist, SCH23390, dose-dependently attenuated cocaine-seeking behavior in an anatomically selective manner, without altering motor performance. Furthermore, the effects of SCH23390 could be surmounted by co-administration of a sub-threshold dose of the D1-like receptor agonist, SKF81297. In experiment 2, we examined effects of D1-like receptor antagonism in the OFC on OFC-BLA interactions using a functional disconnection manipulation. Unilateral SCH23390 administration into the OFC plus GABA agonist-induced neural inactivation of the contralateral or ipsilateral BLA disrupted drug context-induced cocaine-seeking behavior relative to vehicle, while independent unilateral manipulations of these brain regions were without effect. Finally, in experiment 3, we used fluorescent retrograde tracers to demonstrate that the VTA, but not the substantia nigra, sends dense intra-and interhemispheric projections to the OFC, which in turn has reciprocal bi-hemispheric connections with the BLA. These findings support that dopaminergic input from the VTA, via dopamine D1-like receptor stimulation in the OFC, is required for OFC-BLA functional interactions. Thus, a VTA-OFC-BLA neural circuit promotes drug context-induced motivated behavior.

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Section: Introductionmentioning

confidence: 99%

Contribution of a Mesocorticolimbic Subcircuit to Drug Context-Induced Reinstatement of Cocaine-Seeking Behavior in Rats

Lasseter

Xie

Arguello

et al. 2013

Neuropsychopharmacol

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“…Dopamine D2 receptor antagonism impaired set-shifting, while inhibition of the D4 receptor (a member of the D2-family of dopamine receptors) had opposing effects on behavior (Floresco et al 2006). Furthermore, loss of either the D1 or D2 receptor activity in the mPFC can prevent the ability to update behavior in response to changes in reward value, but does not appear to block perception of the value change (Winter et al 2009). While these data are not specific to IL, they highlight the importance of considering neuromodulator signaling carefully in complex assessments of behavioral flexibility.…”

Section: Infralimbic Pfc Controls Extinction Of Instrumental and Pavlmentioning

confidence: 99%

A unifying model of the role of the infralimbic cortex in extinction and habits

2014

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The infralimbic prefrontal cortex (IL) has been shown to be critical for the regulation of flexible behavior, but its precise function remains unclear. This region has been shown to be critical for the acquisition, consolidation, and expression of extinction learning, leading many to hypothesize that IL suppresses behavior as part of a "stop" network. However, this framework is at odds with IL function in habitual behavior in which the IL has been shown to be required for the expression and acquisition of ongoing habitual behavior. Here, we will review the current state of knowledge of IL anatomy and function in behavioral flexibility and provide a testable framework for a single IL mechanism underlying its function in both extinction and habit learning.Addiction is characterized both by the inability to terminate or reduce drug taking even in the face of adverse consequences and by chronic relapse to drug taking. Investigation into the neurobiological substrates of the loss of behavioral flexibility in addiction has relied heavily on animal models of addictive behavior, including habit and extinction learning paradigms that investigate distinct components of inflexible behavior.The prefrontal cortex (PFC) has repeatedly been identified as critical for the cognitive control of flexible actions (Jentsch and Taylor 1999;Everitt et al. 2008;George and Koob 2010;Willcocks and McNally 2012). Subregions of the PFC have distinct connectivity that likely underlies their separable roles in behavior. The infralimbic PFC (IL) has been shown to have a unique role in the development and expression of inflexible reward seeking. Interestingly, IL has been shown to have opposing effects on behavior when compared with the adjacent prelimbic PFC (PL) or, more broadly, the dorsomedial PFC (dmPFC). Perhaps most surprising are the apparently contradictory roles of IL in different measures of behavioral flexibility. In the current review, we discuss models of inflexible drug seeking and the role of IL in the regulation of these behavioral processes. In particular, we focus on the precise function of IL in the acquisition and extinction of drug seeking and the development and expression of habitual drug-seeking behavior. We propose a framework for reconciling the seemingly contradictory role of IL in the regulation of flexible reward seeking through the suppression of the ability of established action-outcome contingencies to guide behavior.

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“…SCH23390 hydrochloride (Tocris Bioscience) dissolved in sterile 0.9% saline solution (Aquapharm) was administered at a concentration of 5 mM per hemisphere based on previous studies (Seamans et al 1998;Romanides et al 1999;Baldwin et al 2002;Izquierdo et al 2007;Winter et al 2009). SKF83566 hydrobromide (Tocris Bioscience) dissolved in sterile saline (0.9%) was administered at a concentration of 200 mM per hemisphere.…”

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confidence: 99%

Regionally selective requirement for D₁/D₅ dopaminergic neurotransmission in the medial prefrontal cortex in object-in-place associative recognition memory

2015

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Object-in-place (OiP) memory is critical for remembering the location in which an object was last encountered and depends conjointly on the medial prefrontal cortex, perirhinal cortex, and hippocampus. Here we examined the role of dopamine D 1 /D 5 receptor neurotransmission within these brain regions for OiP memory. Bilateral infusion of D 1 /D 5 receptor antagonists SCH23390 or SKF83566 into the medial prefrontal cortex, prior to memory acquisition, impaired OiP performance following a 5 min or 1 h delay. Retrieval was unaffected. Intraperirhinal or intrahippocampal infusions of SCH23390 had no effect. These results reveal a selective role for D 1 /D 5 receptors in the mPFC during OiP memory encoding.Object-in-place (OiP) associative recognition memory involves the formation of an association between an object and the location in which it was last encountered (Gaffan and Parker 1996; Dix and Aggleton 1999) and is therefore a key component of event memory (Mecklinger and Meinshausen 1998). The medial prefrontal cortex (mPFC), perirhinal cortex (PRH), and hippocampus (HPC), comprise an associative recognition memory neural circuit (Gaffan 1994;Browning et al. 2005;Barker et al. 2007;Bachevalier and Nemanic 2008;Barker and Warburton 2013;Lee and Park 2013). However, the neural mechanisms, which underlie the formation of OiP memory, are currently underexplored. The mPFC, PRH, and HPC all receive prominent dopaminergic innervation (Berger et al. 1974;Scatton et al. 1980;Swanson 1982;Sobel and Corbett 1984;Fallon and Laughlin 1995;DiChiara 2002) and exposure to novel stimuli and novel environments increases midbrain dopaminergic cell body firing (Feenstra et al. 1995;Beaufour et al. 2001;De Leonibus et al. 2006). Chao et al. (2013) recently reported that a unilateral forebrain dopamine lesion combined with a unilateral mPFC lesion significantly impaired OiP memory. Thus dopamine is a strong candidate for driving novelty processing, critical during recognition memory. Dopamine acts through different receptor subtypes (D 1 -D 5 ) located within the mPFC, HPC, and PRH, and intra-PRH infusion of the D 1 /D 5 receptor antagonist SCH23390 impaired object recognition after 24 h but not 90 min (Balderas et al. 2013). Thus here we examined the importance of D 1 /D 5 receptor neurotransmission, selectively within the mPFC, PRH, and HPC, during recognition memory encoding or retrieval.Rats were implanted with bilateral cannulae aimed at the mPFC, HPC, or PRH to allow direct intracerebral administration of the D 1 /D 5 receptor antagonists SCH23390 or SKF83566. All animal procedures were performed in accordance with the United Kingdom Animals Scientific Procedures Act (1986) and associated guidelines. Details of the surgery, infusion procedures, behavioral testing, and histology have been published previously (Barker and Warburton 2008). Briefly, male Dark Agouti rats (230-250 g; Harlan, UK) housed under a 12-h/12-h light/dark cycle (light phase 18:00-6:00 h), were anesthetized with isoflurane (induction 4%, maintenance 2%-3%) ...

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Dopamine in the prefrontal cortex regulates rats behavioral flexibility to changing reward value

Cited by 49 publications

References 51 publications

Contribution of a Mesocorticolimbic Subcircuit to Drug Context-Induced Reinstatement of Cocaine-Seeking Behavior in Rats

Contribution of a Mesocorticolimbic Subcircuit to Drug Context-Induced Reinstatement of Cocaine-Seeking Behavior in Rats

A unifying model of the role of the infralimbic cortex in extinction and habits

Regionally selective requirement for D₁/D₅ dopaminergic neurotransmission in the medial prefrontal cortex in object-in-place associative recognition memory

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Dopamine in the prefrontal cortex regulates rats behavioral flexibility to changing reward value

Cited by 49 publications

References 51 publications

Contribution of a Mesocorticolimbic Subcircuit to Drug Context-Induced Reinstatement of Cocaine-Seeking Behavior in Rats

Contribution of a Mesocorticolimbic Subcircuit to Drug Context-Induced Reinstatement of Cocaine-Seeking Behavior in Rats

A unifying model of the role of the infralimbic cortex in extinction and habits

Regionally selective requirement for D1/D5 dopaminergic neurotransmission in the medial prefrontal cortex in object-in-place associative recognition memory

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About

Regionally selective requirement for D₁/D₅ dopaminergic neurotransmission in the medial prefrontal cortex in object-in-place associative recognition memory