Opioid site in nucleus accumbens shell mediates eating and hedonic ‘liking’ for food: map based on microinjection Fos plumes

Peciña, Susana; Berridge, Kent

doi:10.1016/s0006-8993(00)02102-8

Cited by 354 publications

(243 citation statements)

References 69 publications

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“…Our rostral shell region for GABAergic eating behavior overlaps considerably with an earlier map by our laboratory of an opioid eating site in the shell, in which morphine microinjection caused increased food intake (Peciña and Berridge, 2000). However, the appetitive opioid eating site of Peciña and Berridge (ϩ1.0 to ϩ2.2 mm anterior to bregma) also extended posteriorly into our caudal shell region in which GABAergic muscimol elicited negative defensive burying.…”

Section: Functional Interaction Between Neuroanatomical and Neurochemsupporting

confidence: 67%

Fear and Feeding in the Nucleus Accumbens Shell: Rostrocaudal Segregation of GABA-Elicited Defensive Behavior Versus Eating Behavior

2001

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This study examined localization of positive versus negative motivational functions mediated by GABA circuits within the accumbens shell. Microinjections of a GABA A agonist (0, 25, 75, and 225 ng/0.5 l muscimol) in rostral shell sites elicited appetitive increases in eating behavior. In contrast, microinjections in caudal shell sites elicited defensive burying or pawtreading behavior. Rats whose microinjections landed bilaterally outside of the accumbens shell did not display either behavior. Defensive treading elicited by caudal shell muscimol microinjection appeared to be a negative motivated response to threat (similar in parameters and orientation to normal defensive burying of a threatening electrified shock prod). The nucleus accumbens shell thus appears functionally heterogeneous in coding motivational valence. The demonstration that muscimol elicits positive eating behavior from rostral shell versus negative defensive behavior from caudal shell suggests in particular that GABAergic substrates of positive and negative types of motivated behavior in the nucleus accumbens shell are segregated along a rostrocaudal gradient.Key words: accumbens shell; GABA; food intake; reward; appetite; motivation; glutamate; dopamine; fear; defense; aggression; mesolimbic; microinjection GABAergic medium spiny neurons in the nucleus accumbens shell are implicated in the control of appetitive behavior and reward. Regarding eating behavior specifically, robust increases in food intake by rats are elicited by microinjection in the medial accumbens shell of either GABA A or GABA B receptor agonists (or non-NMDA glutamate antagonists) (Maldonado-Irizarry et al., 1995;Stratford and Kelley, 1997;Basso and Kelley, 1999).Aside from its role in positive appetitive behavior, the accumbens shell has also been implicated in negative motivational states, such as stress, fear, and defensive behavioral responses elicited by noxious or threatening stimuli (Inoue et al

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Section: Functional Interaction Between Neuroanatomical and Neurochemsupporting

confidence: 67%

Fear and Feeding in the Nucleus Accumbens Shell: Rostrocaudal Segregation of GABA-Elicited Defensive Behavior Versus Eating Behavior

2001

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“…All rats in Experiment 2 received infusions of the mu-opioid agonist DAMGO at a dose of 0.5 g/l and a flow rate of 0.25 l/min with a 2 min diffusion period. Doses were chosen based on studies of central infusions of opioids in the PAG and NacS (Peciña and Berridge, 2000;Iordanova et al, 2006). Unilateral infusions in the PAG of 0.5 l were performed with the injector extending 1 mm below the guide cannulae for 2 min.…”

Section: Methodsmentioning

confidence: 99%

Free-Operant Avoidance Behavior by Rats after Reinforcer Revaluation Using Opioid Agonists and d-Amphetamine

et al. 2014

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The associative processes that support free-operant instrumental avoidance behavior are still unknown. We used a revaluation procedure to determine whether the performance of an avoidance response is sensitive to the current value of the aversive, negative reinforcer. Rats were trained on an unsignaled, free-operant lever press avoidance paradigm in which each response avoided or escaped shock and produced a 5 s feedback stimulus. The revaluation procedure consisted of noncontingent presentations of the shock in the absence of the lever either paired or unpaired with systemic morphine and in a different cohort with systemic D-amphetamine. Rats were then tested drug free during an extinction test. In both the D-amphetamine and morphine groups, pairing of the drug and shock decreased subsequent avoidance responding during the extinction test, suggesting that avoidance behavior was sensitive to the current incentive value of the aversive negative reinforcer. Experiment 2 used central infusions of D-Ala 2 , NMe-Phe 4 , Gly-ol 5 ]-enkephalin (DAMGO), a mu-opioid receptor agonist, in the periacqueductal gray and nucleus accumbens shell to revalue the shock. Infusions of DAMGO in both regions replicated the effects seen with systemic morphine. These results are the first to demonstrate the impact of revaluation of an aversive reinforcer on avoidance behavior using pharmacological agents, thereby providing potential therapeutic targets for the treatment of avoidance behavior symptomatic of anxiety disorders.

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“…Moreover, drugs that enhance operant responding for such food rewards, such as amphetamine, are most effective when administered into the NAc, whereas DA receptor antagonists administered into the NAc block the stimulant effects [57,311]. Pharmacological control of the output from the NAc shell can also have profound effects on food consumption [312,313], as does surgical or chemical lesion of the nigrostriatal or mesolimbic DA pathways. These results suggest that DA release in the striatum is required to integrate relevant signals for sustained feeding [301,314,315].…”

Section: Reviewmentioning

confidence: 99%

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Dichter

Damiano

Allen

2012

J Neurodevelop Disord

253

207

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This review summarizes evidence of dysregulated reward circuitry function in a range of neurodevelopmental and psychiatric disorders and genetic syndromes. First, the contribution of identifying a core mechanistic process across disparate disorders to disease classification is discussed, followed by a review of the neurobiology of reward circuitry. We next consider preclinical animal models and clinical evidence of reward-pathway dysfunction in a range of disorders, including psychiatric disorders (i.e., substance-use disorders, affective disorders, eating disorders, and obsessive compulsive disorders), neurodevelopmental disorders (i.e., schizophrenia, attention-deficit/hyperactivity disorder, autism spectrum disorders, Tourette’s syndrome, conduct disorder/oppositional defiant disorder), and genetic syndromes (i.e., Fragile X syndrome, Prader–Willi syndrome, Williams syndrome, Angelman syndrome, and Rett syndrome). We also provide brief overviews of effective psychopharmacologic agents that have an effect on the dopamine system in these disorders. This review concludes with methodological considerations for future research designed to more clearly probe reward-circuitry dysfunction, with the ultimate goal of improved intervention strategies.

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Opioid site in nucleus accumbens shell mediates eating and hedonic ‘liking’ for food: map based on microinjection Fos plumes

Cited by 354 publications

References 69 publications

Fear and Feeding in the Nucleus Accumbens Shell: Rostrocaudal Segregation of GABA-Elicited Defensive Behavior Versus Eating Behavior

Fear and Feeding in the Nucleus Accumbens Shell: Rostrocaudal Segregation of GABA-Elicited Defensive Behavior Versus Eating Behavior

Free-Operant Avoidance Behavior by Rats after Reinforcer Revaluation Using Opioid Agonists and d-Amphetamine

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

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