Ventral striatal control of appetitive motivation: role in ingestive behavior and reward-related learning.

By A. Kelley. Neuroscience and Biobehavioral Reviews, 2004

940 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Endocrine and Autonomic Systems, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/94db002f02b6e49b6b7b389efd87a11bdcb6d584

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Citations in the corpus

Activation of VTA GABA neurons disrupts reward consumption (2012, positive): “In addition to VTA GABA neurons signaling locally within the VTA, they also send long distance projections to forebrain targets such as the NAc (Van Bockstaele and Pickel, 1995), a brain region critical for consummatory behaviors (Hanlon et al., 2004; Kelley, 2004; Krause et al., 2010).”
Individual Differences in Reward Drive Predict Neural Responses to Images of Food (2006, background): “Comparative research has implicated a network of interconnected brain regions comprising frontal, ventral striatal, amygdala, and midbrain regions in aspects of food reward (Berridge, 1996, 2003; Ikemoto and Panksepp, 1999; Kelley, 2004; Balleine, 2005; Di Chiara, 2005; Kelley et al., 2005).”
‘Liking’ and ‘wanting’ food rewards: Brain substrates and roles in eating disorders (2009, background): “Widely spread opioid mechanisms for ‘wanting’ in the nucleus accumbens is consistent with previous findings that opioids stimulate food ‘wanting’ throughout the entire nucleus accumbens and even in outside structures that include amygdala or neostriatum [48,50,52,78,79].”
The tempted brain eats: pleasure and desire circuits in obesity and eating disorders. (2010, background): “Physiological hunger ormesolimbic reactivity is important because the motivating power of a cue encounter changes with hunger or satiety (or may vary across individuals due to differences in their brains) (Zhang et al., 2009).”
An Evolutionary Framework to Understand Foraging, Wanting, and Desire: The Neuropsychology of the SEEKING System (2012, background): “There is abundant evidence for such mechanisms in the basal ganglia, especially in the nucleus accumbens (Kelley, 1999a, 1999b).”
Human and Rodent Homologies in Action Control: Corticostriatal Determinants of Goal-Directed and Habitual Action (2010, background): “Kelley AE (2004). Ventral striatal control of appetitive motivation: role in ingestive”
The 7R polymorphism in the dopamine receptor D4 gene (DRD4) is associated with financial risk taking in men (2009, background): “These pathways play a role in regulating the anticipation of rewards (Kelley, Schiltz, & Landry, 2005; Wise, 2002) as well as the motivation for obtaining rewards (Kelley, 2004) and include the ventral tegmental area, nucleus accumbens, and the prefrontal cortex.”
The debate over dopamine’s role in reward: the case for incentive salience (2007, methodology): “…glutamate-coded signals at the cellular and molecular level is a fundamental event underlying long-term plasticity and reward-related learning... " (Kelley 2004a, p. 166) or " Dopamine neurons appear to emit a reward prediction error signal... " (Schultz 2004, p. 4) or " We have presented…”
Widespread reward-system activation in obese women in response to pictures of high-calorie foods (2008, positive): “Furthermore, in animal studies pharmacological manipulations of the NAc have been found to stimulate food intake (Kelley, 2004; Smith and Berridge, 2007).”
Effort-related functions of nucleus accumbens dopamine and associated forebrain circuits (2007, background): “This point has been highlighted in the work of Kelley (e.g., Smith-Roe and Kelley 2000, 2004; Kelley et al. 2005).”
Structural plasticity associated with exposure to drugs of abuse. (2004, positive): “Many of the structures in which we have seen drug-induced changes in dendritic structure are brain regions that have been implicated in various aspects of learning (Cardinal et al., 2002; Killcross and Coutureau, 2003; Cardinal and Everitt, 2004; Holland and Gallagher, 2004; Kelley, 2004).”
Hedonic Hot Spot in Nucleus Accumbens Shell: Where Do μ-Opioids Cause Increased Hedonic Impact of Sweetness? (2005, background): “…thought to participate in generating hedonic impact for drug rewards and for natural sensory pleasures such as sweetness (Zhang et al., 1998; Peciña and Berridge, 2000; Kelley et al., 2002, 2004; Robbins and Everitt, 2002; Berridge, 2003; Koob, 2003; Bodnar et al., 2005; Kalivas and Volkow, 2005).”