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      Hedonic sensitivity to natural rewards is affected by prenatal stress in a sex-dependent manner : Early stress, sex and reward

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          Most cited references 83

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          Dysfunction of the prefrontal cortex in addiction: neuroimaging findings and clinical implications.

          The loss of control over drug intake that occurs in addiction was initially believed to result from disruption of subcortical reward circuits. However, imaging studies in addictive behaviours have identified a key involvement of the prefrontal cortex (PFC) both through its regulation of limbic reward regions and its involvement in higher-order executive function (for example, self-control, salience attribution and awareness). This Review focuses on functional neuroimaging studies conducted in the past decade that have expanded our understanding of the involvement of the PFC in drug addiction. Disruption of the PFC in addiction underlies not only compulsive drug taking but also accounts for the disadvantageous behaviours that are associated with addiction and the erosion of free will.
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            Environmental contributions to the obesity epidemic.

            The current epidemic of obesity is caused largely by an environment that promotes excessive food intake and discourages physical activity. Although humans have evolved excellent physiological mechanisms to defend against body weight loss, they have only weak physiological mechanisms to defend against body weight gain when food is abundant. Control of portion size, consumption of a diet low in fat and energy density, and regular physical activity are behaviors that protect against obesity, but it is becoming difficult to adopt and maintain these behaviors in the current environment. Because obesity is difficult to treat, public health efforts need to be directed toward prevention.
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              Neurocircuitry of addiction.

              Drug addiction is a chronically relapsing disorder that has been characterized by (1) compulsion to seek and take the drug, (2) loss of control in limiting intake, and (3) emergence of a negative emotional state (eg, dysphoria, anxiety, irritability) reflecting a motivational withdrawal syndrome when access to the drug is prevented. Drug addiction has been conceptualized as a disorder that involves elements of both impulsivity and compulsivity that yield a composite addiction cycle composed of three stages: 'binge/intoxication', 'withdrawal/negative affect', and 'preoccupation/anticipation' (craving). Animal and human imaging studies have revealed discrete circuits that mediate the three stages of the addiction cycle with key elements of the ventral tegmental area and ventral striatum as a focal point for the binge/intoxication stage, a key role for the extended amygdala in the withdrawal/negative affect stage, and a key role in the preoccupation/anticipation stage for a widely distributed network involving the orbitofrontal cortex-dorsal striatum, prefrontal cortex, basolateral amygdala, hippocampus, and insula involved in craving and the cingulate gyrus, dorsolateral prefrontal, and inferior frontal cortices in disrupted inhibitory control. The transition to addiction involves neuroplasticity in all of these structures that may begin with changes in the mesolimbic dopamine system and a cascade of neuroadaptations from the ventral striatum to dorsal striatum and orbitofrontal cortex and eventually dysregulation of the prefrontal cortex, cingulate gyrus, and extended amygdala. The delineation of the neurocircuitry of the evolving stages of the addiction syndrome forms a heuristic basis for the search for the molecular, genetic, and neuropharmacological neuroadaptations that are key to vulnerability for developing and maintaining addiction.
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                Author and article information

                Journal
                Addiction Biology
                Addiction Biology
                Wiley
                13556215
                November 2016
                November 2016
                May 26 2015
                : 21
                : 6
                : 1072-1085
                Affiliations
                [1 ]International Associated Laboratory (LIA) ‘Prenatal Stress and Neurodegenerative Diseases’; UMR8576 University Lille 1/CNRS; France
                [2 ]Sapienza University of Rome/IRCCS Neuromed; Italy
                [3 ]IRCCS; Centro Neurolesi ‘Bonino-Pulejo’; Italy
                [4 ]Advanced Molecular Diagnostic; Sant'Andrea Hospital; Italy
                [5 ]EA4483; University Lille 2; France
                [6 ]Institute of Neuroscience; National Research Council (CNR); Italy
                [7 ]Genomnia; Italy
                [8 ]Department of Pharmacy; University of Genoa; Italy
                Article
                10.1111/adb.12270
                26011513
                © 2015
                Product
                Self URI (article page): http://doi.wiley.com/10.1111/adb.12270

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