Orbitofrontal and striatal circuits dynamically encode the shift between goal-directed and habitual actions

Gremel, Christina M.; Costa, Rui M.

doi:10.1038/ncomms3264

Cited by 553 publications

(690 citation statements)

References 58 publications

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“…Indeed, lateral OFC pyramidal neurons from extended access rats had a depolarized resting membrane potential. Consistent with our results, optogenetic stimulation of CaMKII-containing OFC neurons leads to increased lever pressing for sucrose in the satiety-induced devalued state (Gremel and Costa, 2013).…”

Section: Gaba Onto Pyramidal Neurons Of the Lateral Ofcsupporting

confidence: 78%

“…OFC function has been implicated in the devaluation of food rewards either by satiety (Gremel and Costa, 2013;Rudebeck et al, 2013), sickness paired cues (Schoenbaum et al, 2003) or by changing the action contingency (Ostlund and Balleine, 2007). Therefore, we hypothesized that a cafeteria diet may induce changes in lateral OFC pyramidal neurons.…”

Section: Resultsmentioning

confidence: 99%

“…Given that the OFC receives significant sensory information and contains neurons that respond to taste and olfaction (Rolls, 2012), the OFC likely integrates signals about the sensory properties of food (taste, texture, smell) with expected outcomes. OFC lesions or inactivation are associated with impairment in either satiety-induced (Gremel and Costa, 2013;Rudebeck et al, 2013) or LiCl (sickness)-induced food devaluation (Schoenbaum et al, 2003). Thus, the OFC registers the current value of foods and updates actions based on this information.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Obesity-Induced Structural and Neuronal Plasticity in the Lateral Orbitofrontal Cortex

Thompson

Drysdale

Baimel

et al. 2017

Neuropsychopharmacol

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The orbitofrontal cortex (OFC) integrates sensory information with the current value of foods and updates actions based on this information. Obese humans and rats fed a cafeteria diet have impaired devaluation of food rewards, implicating a potential obesity-induced dysfunction of the OFC. We hypothesized that obesity alters OFC © 2016 Macmillan Publishers Limited. All rights reserved. 3pyramidal neuronal structure and function and reduces conditioned suppression of feeding. Rats were given restricted (1 h/day), extended (23 h/day) or no (chow only) access to a cafeteria diet and tested for a conditioned suppression of feeding. Golgicox impregnation and whole-cell patch clamp experiments were performed in lateral OFC pyramidal neurons of rats from the 3 feeding groups. Rats with 40 days of extended, but not restricted, access to a cafeteria diet became obese and continued to feed during foot shock-predicting cues. Access to a cafeteria diet induced morphological changes in basilar dendrites of lateral OFC pyramidal neurons. While there were no alterations in excitatory synaptic transmission underlying altered spine density, we observed a more depolarized resting membrane potential. This was accompanied by decreased inhibitory synaptic transmission onto lateral OFC pyramidal neurons due to decreased release probability at GABAergic inputs. These changes could underlie the inability of the OFC to encode changes in the motivation value of food that is observed in obese rodents and humans.

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Section: Gaba Onto Pyramidal Neurons Of the Lateral Ofcsupporting

confidence: 78%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Obesity-Induced Structural and Neuronal Plasticity in the Lateral Orbitofrontal Cortex

Thompson

Drysdale

Baimel

et al. 2017

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…Therefore, the failure to observe selective devaluation after a 5 hour delay does not indicate that instrumental behavior is governed by habitual S-R processes. Instead, our results provide evidence that contextual cues may be required for the value of specific outcomes to control instrumental responding; a suggestion that is consistent with several recent reports that the context can modulate instrumental behavior (Gremel & Costa, 2013;Jonkman, Kosaki, Everitt, & Dickinson, 2010;Thrailkill & Bouton, 2015;Todd, Winterbauer, & Bouton, 2012).…”

Section: Discussionsupporting

confidence: 79%

A time course analysis of satiety-induced instrumental outcome devaluation

2016

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Sensory-specific satiety is commonly used in studies of decision making to selectively devalue a food reward. Devaluation is reflected in an immediate reduction in the subsequent intake of the food and in the performance of actions that gain access to that food. Despite its frequent use, the lasting effects of satiety-induced devaluation on instrumental actions are unknown. Here, we examined the time course and contextual dependency of sensory-specific satiety-induced devaluation on instrumental responding and consumption. Rats were trained to perform two instrumental actions for two distinct food rewards. Then, one of the instrumental outcomes was provided ad libitum for 1 hour in separate feeding cages and the effect of this devaluation was assessed 0, 2, or 5 hours after satiation. At a delay of 0 or 2 hours, both intake and instrumental responding were sensitive to the satiety treatment. That is, rats consumed less of the devalued outcome and responded less for the devalued outcome than for the valued outcome. By contrast, after 5 hours, rats showed sensitivity to devaluation in consumption but not in instrumental responding. Strikingly, sensitivity to devaluation was restored for the instrumental response after a 5 hour delay when devaluation was performed in the instrumental context. These results indicate that, in rats, specific satiety-induced devaluation endures and is context-independent for up to 2 hours postsatiation. At longer delays, the impact of sensory-specific satiety on instrumental responding is context-dependent, suggesting that contextual cues may be required for the value of specific outcomes to control instrumental responding.

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“…The eCB system appears to modulate several phenomena related to addiction, including drug-induced reward, the motivation to procure the drug and behavioral sensitization (Vinod et al 2008). CB1Rs are highly expressed in the dorsolateral striatum (DLS), a critical brain region for the gradual acquisition of habitual and automatic behaviors (Gremel & Costa 2013). Striatal CB1Rs may thus be crucial for establishing behavioral patterns that are directed compulsively toward drug usage (Gerdeman et al 2003).…”

Section: Introductionmentioning

confidence: 99%

Acute and chronic modulation of striatal endocannabinoid‐mediated plasticity by nicotine

et al. 2018

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The endocannabinoid (eCB) system modulates several phenomena related to addictive behaviors, and drug-induced changes in eCB signaling have been postulated to be important mediators of physiological and pathological rewardrelated synaptic plasticity. Here, we studied eCB-mediated long-term depression (eCB-LTD) in the dorsolateral striatum, a brain region critical for acquisition of habitual and automatic behavior. We report that nicotine differentially affects ex vivo eCB signaling depending on previous exposure in vivo. In the nicotine-naïve brain, nicotine facilitates eCB-signaling and LTD, whereas tolerance develops to this facilitating effect after subchronic exposure in vivo. In the end, a progressive impairment of eCB-induced LTD is established after protracted withdrawal from nicotine. Endocannabinoid-LTD is reinstated 6 months after the last drug injection, but a brief period of nicotine re-exposure is sufficient to yet again impair eCB-signaling. LTD induced by the cannabinoid 1 receptor agonist WIN55,212-2 is not affected, suggesting that nicotine modulates eCB production or release. Nicotine-induced facilitation of eCB-LTD is occluded by the dopamine D2 receptor agonist quinpirole, and by the muscarinic acetylcholine receptor antagonist scopolamine. In addition, the same compounds restore eCB-LTD during protracted withdrawal. Nicotine may thus modulate eCB-signaling by affecting dopaminergic and cholinergic neurotransmission in a long-lasting manner. Overall, the data presented here suggest that nicotine facilitates eCB-LTD in the initial phase, which putatively could promote neurophysiological and behavioral adaptations to the drug. Protracted withdrawal, however, impairs eCB-LTD, which may influence or affect the ability to maintain cessation.

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Orbitofrontal and striatal circuits dynamically encode the shift between goal-directed and habitual actions

Cited by 553 publications

References 58 publications

Obesity-Induced Structural and Neuronal Plasticity in the Lateral Orbitofrontal Cortex

Obesity-Induced Structural and Neuronal Plasticity in the Lateral Orbitofrontal Cortex

A time course analysis of satiety-induced instrumental outcome devaluation

Acute and chronic modulation of striatal endocannabinoid‐mediated plasticity by nicotine

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