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).