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      Actions of feeding-related peptides on the mesolimbic dopamine system in regulation of natural and drug rewards

      research-article
      a , a , b , *
      Addiction neuroscience
      Dopamine, VTA, Feeding, Peptide, Reward, Drugs

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          Abstract

          The mesolimbic dopamine system is the primary neural circuit mediating motivation, reinforcement, and reward-related behavior. The activity of this system and multiple behaviors controlled by it are affected by changes in feeding and body weight, such as fasting, food restriction, or the development of obesity. Multiple different peptides and hormones that have been implicated in the control of feeding and body weight interact with the mesolimbic dopamine system to regulate many different dopamine-dependent, reward-related behaviors. In this review, we summarize the effects of a selected set of feeding-related peptides and hormones acting within the ventral tegmental area and nucleus accumbens to alter feeding, as well as food, drug, and social reward.

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          A neural substrate of prediction and reward.

          The capacity to predict future events permits a creature to detect, model, and manipulate the causal structure of its interactions with its environment. Behavioral experiments suggest that learning is driven by changes in the expectations about future salient events such as rewards and punishments. Physiological work has recently complemented these studies by identifying dopaminergic neurons in the primate whose fluctuating output apparently signals changes or errors in the predictions of future salient and rewarding events. Taken together, these findings can be understood through quantitative theories of adaptive optimizing control.
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            Social reward requires coordinated activity of accumbens oxytocin and 5HT

            Social behaviors in species as diverse as honey bees and humans promote group survival but often come at some cost to the individual. Although reinforcement of adaptive social interactions is ostensibly required for the evolutionary persistence of these behaviors, the neural mechanisms by which social reward is encoded by the brain are largely unknown. Here we demonstrate that in mice oxytocin (OT) acts as a social reinforcement signal within the nucleus accumbens (NAc) core, where it elicits a presynaptically expressed long-term depression of excitatory synaptic transmission in medium spiny neurons. Although the NAc receives OT receptor-containing inputs from several brain regions, genetic deletion of these receptors specifically from dorsal raphe nucleus, which provides serotonergic (5-HT) innervation to the NAc, abolishes the reinforcing properties of social interaction. Furthermore, OT-induced synaptic plasticity requires activation of NAc 5-HT1b receptors, the blockade of which prevents social reward. These results demonstrate that the rewarding properties of social interaction in mice require the coordinated activity of OT and 5-HT in the NAc, a mechanistic insight with implications for understanding the pathogenesis of social dysfunction in neuropsychiatric disorders such as autism.
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              Positive reinforcement produced by electrical stimulation of septal area and other regions of rat brain.

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                Author and article information

                Journal
                9918367980706676
                51511
                Addict Neurosci
                Addict Neurosci
                Addiction neuroscience
                2772-3925
                12 May 2023
                June 2022
                26 February 2022
                22 May 2023
                : 2
                : 100011
                Affiliations
                [a ]Department of Biology and Neuroscience Institute, Georgia State University, Atlanta, GA 30303, USA
                [b ]Neuroscience Institute, Georgia State University, Atlanta, GA 30303, USA
                Author notes
                [* ]Corresponding Author. aroseberry@ 123456gsu.edu (A.G. Roseberry).
                Article
                NIHMS1899538
                10.1016/j.addicn.2022.100011
                10201992
                37220637
                34aefac9-57ec-4e2b-9a88-bb4136a6ec52

                This is an open access article under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/)

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                Categories
                Article

                dopamine,vta,feeding,peptide,reward,drugs
                dopamine, vta, feeding, peptide, reward, drugs

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