Cortico-Basal Ganglia Reward Network: Microcircuitry
By S. Sesack, Anthony A. Grace. Neuropsychopharmacology, 2009
991 citations recorded by the source corpus.
Many of the brain's reward systems converge on the nucleus accumbens, a region richly innervated by excitatory, inhibitory, and modulatory afferents representing the circuitry necessary for selecting adaptive motivated behaviors. The ventral subiculum of the hippocampus provides contextual and spatial information, the basolateral amygdala conveys affective influence, and the prefrontal cortex provides an integrative impact on goal-directed behavior. The balance of these afferents is under the modulatory influence of dopamine neurons in the ventral tegmental area. This midbrain region receives its own complex mix of excitatory and inhibitory inputs, some of which have only recently been identified. Such afferent regulation positions the dopamine system to bias goal-directed behavior based on internal drives and environmental contingencies. Conditions that result in reward promote phasic dopamine release, which serves to maintain ongoing behavior by selectively potentiating ventral subicular drive to the accumbens. Behaviors that fail to produce an expected reward decrease dopamine transmission, which favors prefrontal cortical-driven switching to new behavioral strategies. As such, the limbic reward system is designed to optimize action plans for maximizing reward outcomes. This system can be commandeered by drugs of abuse or psychiatric disorders, resulting in inappropriate behaviors that sustain failed reward strategies. A fuller appreciation of the circuitry interconnecting the nucleus accumbens and ventral tegmental area should serve to advance discovery of new treatment options for these conditions.
Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience
View Paper: https://www.semanticscholar.org/paper/b5d42603c7cedf16d86e4efcb58c29c7d1834c75
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Citations in the corpus
- RETHINKING THE EMOTIONAL BRAIN (2012, neutral): “…1980; Balleine and Killcross, 1994; Killcross and Robbins, 1993; Everitt et al., 1999; Cardinal et al., 2002; Ikemoto and Panksepp, 1999; Parkinson et al., 1999; Koob, 2009; Sesack and Grace, 2010; Berridge, 2007, 2009; Berridge and Robinson, 1998; Hyman et al., 2006; Nestler, 2004; Kelley, 2004).”
- Synaptic and Behavioral Profile of Multiple Glutamatergic Inputs to the Nucleus Accumbens (2012, positive): “Pathway-specific activation of these fibers has been demonstrated to elicit distinct physiological and behavioral responses (Goto and Grace, 2008; Sesack and Grace, 2010).”
- Reward and aversion in a heterogeneous midbrain dopamine system (2013, background): “Afferent control of dopamine neuron activity The VTA receives both excitatory and inhibitory inputs from a broad distribution of brain areas (Geisler et al., 2007; Sesack and Grace 2010; Watabe-Uchida et al., 2012).”
- The Brain on Drugs: From Reward to Addiction. (2015, background): “, 2013) innervate the medial PFC, but not the NAc (Bannon and Roth, 1983; Lammel et al., 2012; Sesack and Grace, 2010).”
- Dopamine release in the basal ganglia (2011, background): “However, the balance between excitatory and inhibitory input differs between SNc and VTA, with predominant GABA input to SNc (Bolam and Smith, 1990) and glutamate input to VTA (Smith et al., 1996; Sesack and Grace 2010).”
- The chronic mild stress (CMS) model of depression: History, evaluation and usage (2016, background): “, 1996), the DA-antidepressant interaction probably occurs indirectly: the ascending 5HT and NA projections terminate within the hippocampus, amygdala and PFC, all of which project to the nucleus accumbens shell, where their projections terminate in partially overlapping fields (French and Totterdel”
- Whole-brain mapping of direct inputs to midbrain dopamine neurons. (2012, neutral): “Electron microscopy can resolve several of these issues (e.g., Bolam and Smith, 1990; Carr and Sesack, 2000; Omelchenko et al., 2009; Omelchenko and Sesack, 2010; Somogyi et al., 1981), but this technique is not suitable for a comprehensive identification of inputs.”
- Drug-evoked synaptic plasticity in addiction: from molecular changes to circuit remodeling (2011, background): “Asmentioned above, NAcMSNs are not homogeneous but, like MSNs in the dorsal striatum, can be divided into two major subpopulations (Kreitzer and Malenka, 2008; Sesack and Grace, 2010; Gertler et al., 2008).”