Opposing roles for the nucleus accumbens core and shell in cue-induced reinstatement of food-seeking behavior

Floresco, Stan; McLaughlin, Ryan J.; Haluk, Desirae M.

doi:10.1016/j.neuroscience.2008.04.004

Cited by 114 publications

(114 citation statements)

References 25 publications

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“…Inactivation of NAcc shell prior to initial discrimination learning improves performance of set shift behavior (Floresco et al 2006) and blocks latent inhibition (Weiner et al 1996;Jongen-Relo et al 2002;Pothuizen et al 2005bPothuizen et al , 2006. The NAcc shell plays a particular role in responses to changes in the incentive value of conditioned stimuli (Floresco et al 2008;Granon and Floresco 2009), which may be important in different forms of behavioral flexibility. Here we investigate the neural mechanisms underlying behavioral flexibility in a task requiring a shift in responses after a contingency switch, using brief optogenetic inhibition to silence NAcc shell neurons in specific time segments.…”

Section: [Supplemental Materials Is Available For This Article]mentioning

confidence: 99%

Behavioral flexibility is increased by optogenetic inhibition of neurons in the nucleus accumbens shell during specific time segments

et al. 2014

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Behavioral flexibility is vital for survival in an environment of changing contingencies. The nucleus accumbens may play an important role in behavioral flexibility, representing learned stimulus -reward associations in neural activity during response selection and learning from results. To investigate the role of nucleus accumbens neural activity in behavioral flexibility, we used light-activated halorhodopsin to inhibit nucleus accumbens shell neurons during specific time segments of a bar-pressing task requiring a win-stay/lose -shift strategy. We found that optogenetic inhibition during action selection in the time segment preceding a lever press had no effect on performance. However, inhibition occurring in the time segment during feedback of results-whether rewards or nonrewards-reduced the errors that occurred after a change in contingency. Our results demonstrate critical time segments during which nucleus accumbens shell neurons integrate feedback into subsequent responses. Inhibiting nucleus accumbens shell neurons in these time segments, during reinforced performance or after a change in contingencies, increases lose -shift behavior. We propose that the activity of nucleus shell accumbens shell neurons in these time segments plays a key role in integrating knowledge of results into subsequent behavior, as well as in modulating lose -shift behavior when contingencies change.

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Section: [Supplemental Materials Is Available For This Article]mentioning

confidence: 99%

Behavioral flexibility is increased by optogenetic inhibition of neurons in the nucleus accumbens shell during specific time segments

et al. 2014

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“…It is notable that the role of the medial shell region of the NAc in this form of decision making has not been investigated directly. Given that the core and shell have been shown to play dissociable roles in other functions mediated by the PFC (Floresco, Ghods-Sharifi, Vexelman, & Magyar, 2006;Floresco, McLaughlin, & Haluk, 2008), it would be of great interest to compare the contributions that these two adjacent regions of the ventral striatum make to risk-based judgments. Nevertheless, these studies suggest that intact NAc functioning biases the direction of an individual choice toward potentially larger rewards, even though they may come with a greater risk.…”

Section: Risk-based Decision Makingmentioning

confidence: 99%

Cortico-limbic-striatal circuits subserving different forms of cost-benefit decision making

Floresco

Onge

Ghods-Sharifi

et al. 2008

Cognitive, Affective, & Behavioral Neuroscience

268

222

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“…All microinjections were made in a volume of 0.5 l per side over 2 min. These volumes and doses have been used in previous studies to inactivate the AcbSh and LH separately from their adjacent brain regions (Floresco et al, 2008;Fuchs et al, 2008;Marchant et al, 2009). After allowing an additional 2 min for diffusion, microinjectors were removed and rats were returned to their home cage for ϳ2 min, before being tested in the self-administration chamber.…”

Section: Microinfusion Proceduresmentioning

confidence: 99%

Accumbens Shell–Hypothalamus Interactions Mediate Extinction of Alcohol Seeking

Millan¹,

Furlong²,

McNally³

2010

J. Neurosci.

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The nucleus accumbens shell (AcbSh) is required to inhibit drug seeking after extinction training. Conversely, the lateral hypothalamus (LH), which receives projections from AcbSh, mediates reinstatement of previously extinguished drug seeking. We hypothesized that reversible inactivation of AcbSh using GABA agonists (baclofen/muscimol) would reinstate extinguished alcohol seeking and increase neuronal activation in LH. Rats underwent self-administration training for 4% (v/v) alcoholic beer followed by extinction. AcbSh inactivation reinstated extinguished alcohol seeking when infusions were made after, but not before, extinction training. We then used immunohistochemical detection of c-Fos as a marker of neuronal activity, combined with immunohistochemical detection of the orexin and cocaine-and amphetamine-related transcript (CART) peptides, to study the profile and phenotype of neural activation during reinstatement produced by AcbSh inactivation. AcbSh inactivation increased c-Fos expression in hypothalamus, as well as in paraventricular thalamus and amygdala. Within hypothalamus, there was an increase in the number of orexin and CART cells expressing c-Fos. Finally, we hypothesized that concurrent inactivation of LH would prevent reinstatement produced by inactivation of AcbSh alone. Our results confirmed this. Together, these findings suggest that AcbSh mediates extinction of reward seeking by inhibiting hypothalamic neuropeptide neurons. Reversible inactivation of the AcbSh removes this influence, thereby releasing hypothalamus from AcbSh inhibition and enabling reinstatement of reward seeking. These ventral striatal-hypothalamic circuits for extinction overlap with those that mediate satiety, and we suggest that extinction training inhibits drug seeking because it co-opts neural circuits originally selected to produce satiety.

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Opposing roles for the nucleus accumbens core and shell in cue-induced reinstatement of food-seeking behavior

Cited by 114 publications

References 25 publications

Behavioral flexibility is increased by optogenetic inhibition of neurons in the nucleus accumbens shell during specific time segments

Behavioral flexibility is increased by optogenetic inhibition of neurons in the nucleus accumbens shell during specific time segments

Cortico-limbic-striatal circuits subserving different forms of cost-benefit decision making

Accumbens Shell–Hypothalamus Interactions Mediate Extinction of Alcohol Seeking

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