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Chunk #46 — 3. Neural Substrates for Increased Drug-taking with Extended Access — 3.2. Between-system neuroadaptations

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Neurobiological substrates for the dark side of compulsivity in addiction.
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et al., 2008b). A focal point for many of these effects is the extended amygdala but at the level of the bed nucleus of the stria terminalis. κ Dynorphin, an opioid peptide that binds to κ opioid receptors, has long been known to show activation with chronic administration of psychostimulants and opioids (Nestler, 2004; Koob, 2008), and κ opioid agonists produce aversive effects in animals and humans (Mucha and Herz, 1985; Pfeiffer et al., 1986). A κ opioid antagonist blocks the excessive drinking associated with ethanol withdrawal and dependence (Walker and Koob, 2008). Evidence demonstrates that κ receptor activation can produce CRF release (Song and Takemori, 1992), but recently some have argued that the effects of dynorphin in producing negative emotional states are mediated via activation of CRF systems (Land et al., 2008).