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Review
. 2002 May 1;22(9):3306-11.
doi: 10.1523/JNEUROSCI.22-09-03306.2002.

The neuroscience of natural rewards: relevance to addictive drugs

Ann E Kelley  1 , Kent C Berridge
Affiliations
Review

The neuroscience of natural rewards: relevance to addictive drugs

Ann E Kelley et al. J Neurosci. .
No abstract available

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Figures

Fig. 1.
Fig. 1.
Naturalistic behavior assays of reward liking and negative fearful defense. Liking facial expressions are elicited by the taste of sucrose from newborn human infants, orangutans, and rats [top left, facial photographs fromSteiner et al. (2001) and Berridge (2000)]. Disliking expressions are elicited by the taste of quinine. NAc coronal map of opioid liking and wanting sites for food reward shows intensity of food wanting produced by morphine microinjections in the shell [bottom left, Peciña and Berridge (2000)]. Accompanying graph shows the increase in sucrose liking reactions caused by morphine microinjections in the accumbens shell. Conversely, anxiogenic and psychotic effects of addictive drugs may be related to natural fearful active defense reactions (right). Fearful defensive treading is elicited naturally from rodents by rattlesnake predators and centrally by GABA agonist microinjections in the caudal accumbens shell [California ground squirrel photograph by John Cooke from Coss and Owings (1989); rat photograph from Reynolds and Berridge (2001)]. Bar graph shows elicitation of fearful defensive treading along a rostrocaudal gradient in the NAc shell after GABA agonist microinjections (Reynolds and Berridge, 2001). Separate mesocorticolimbic channels for appetitive and aversive motivational functions is suggested by sagittal map of NAc shell rostrocaudal segregation of GABA-elicited positive feeding behavior (anteriorx symbols) versus fearful defensive behavior (posterior squares).
Fig. 2.
Fig. 2.
Schematic representation of rat brain sagittal section depicting pathways involved in processing of natural rewards and in neural plasticity underlying reward-related learning. Circuitry represented in blue indicates long glutamatergic pathways between prefrontal cortex (PFC), amygdala (Amyg), hippocampus (Hipp), ventral striatum (nucleus accumbens), and ventral tegmental area (VTA). Red circuitry represents principal ascending mesocorticolimbic dopamine systems. Greendescending pathways indicate primarily GABAergic descending systems.Triangles in corresponding colors indicate similar DA, glutamate, and GABAergic coding in dorsal striatum.Violet-shaded boxes represent important nodes within this distributed network where NMDA/D1 receptor-mediated plasticity is proposed to be a critical substrate for behavioral adaptation and learning. For purposes of simplicity, not all relevant circuitry is shown; for example, there are important connections between hypothalamus and amygdala, and glutamatergic thalamic inputs are not shown. Drawing of section is based on the atlas of Paxinos and Watson (1998). Large arrows indicate flow of effector pathways converging on viscero–endocrine and autonomic systems (emerging from hypothalamus and amygdala) and somatic voluntary motor systems (emerging from basal ganglia and ventral midbrain).Inset reflects intracellular and genomic mechanisms hypothesized to govern DA- and glutamate-dependent plasticity within the indicated (violet shaded) nodes. Such plasticity, which may result in altered network activity, is hypothesized to mediate normal learning and memory related to natural rewards but is also a key component of addiction. AcbC, Accumbens core;Acb shell, accumbens shell; Cpu, caudate–putamen; VP, ventral pallidum;Hypo, hypothalamus; SN, substantia nigra. Other abbreviations can be found in Paxinos and Watson (1998).
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References

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