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FIGURE 1–3. Sagittal section through a representative rodent brain illustrating the pathways and receptor systems implicated in the acute reinforcing actions of drugs of abuse.

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FIGURE 1–3. Sagittal section through a representative rodent brain illustrating the pathways and receptor systems implicated in the acute reinforcing actions of drugs of abuse.Cocaine and amphetamines activate the release of dopamine in the nucleus accumbens and amygdala via direct actions on dopamine terminals. Opioids activate opioid receptors in the ventral tegmental area, nucleus accumbens, and amygdala via direct actions on interneurons. Opioids facilitate the release of dopamine in the nucleus accumbens via an action either in the ventral tegmental area or the nucleus accumbens, but are also hypothesized to activate elements independent of the dopamine system. Alcohol activates -aminobutyric acidA (GABAA) receptors in the ventral tegmental area, nucleus accumbens, and amygdala via either direct actions at the GABAA receptor or through indirect release of GABA. Alcohol is hypothesized to facilitate the release of opioid peptides in the ventral tegmental area, nucleus accumbens, and central nucleus of the amygdala. Alcohol facilitates the release of dopamine in the nucleus accumbens via an action either in the ventral tegmental area or the nucleus accumbens. Nicotine activates nicotinic acetylcholine receptors in the ventral tegmental area, nucleus accumbens, and amygdala, either directly or indirectly, via actions on interneurons. Nicotine may also activate opioid peptide release in the nucleus accumbens or amygdala, independent of the dopamine system. Cannabinoids activate cannabinoid type 1 (CB1) receptors in the ventral tegmental area, nucleus accumbens, and amygdala via direct actions on interneurons. Cannabinoids facilitate the release of dopamine in the nucleus accumbens via an action either in the ventral tegmental area or the nucleus accumbens, but are also hypothesized to activate elements independent of the dopamine system. Endogenous cannabinoids may interact with postsynaptic elements in the nucleus accumbens involving dopamine and/or opioid peptide systems. The blue arrows represent the interactions within the extended amygdala system hypothesized to have a key role in psychostimulant reinforcement. AC = anterior commissure; AMG = amygdala; ARC = arcuate nucleus; BNST = bed nucleus of the stria terminalis; Cer = cerebellum; C-P = caudate-putamen; DMT = dorsomedial thalamus; FC = frontal cortex; Hippo = hippocampus; IF = inferior colliculus; LC = locus coeruleus; LH = lateral hypothalamus; N Acc = nucleus accumbens; OT = olfactory tract; PAG = periaqueductal gray; RPn = reticular pontine nucleus; SC = superior colliculus; SNr = substantia nigra pars reticulata; VP = ventral pallidum; VTA = ventral tegmental area.Source. Reprinted from Koob GF: "The Neurocircuitry of Addiction: Implications for Treatment." Clinical Neuroscience Research 5:89–101, 2005. Used with permission.

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