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It was hypothesized that a metabolite of morphine, morphine-3-glucuronide (M3G), contributes to the expression of symptoms seen during withdrawal from morphine. To test this hypothesis, the behaviors observed during precipitated withdrawal from morphine and sufentanil were compared. Sufentanil was chosen because, like morphine, it acts primarily at the mu opioid receptor, but has different metabolites. Differences in the abstinence syndromes produced by the two drugs may therefore be attributable to the actions of metabolites, rather than the primary opioid actions of morphine and sufentanil. Although there were some differences in the occurrence of symptoms, morphine and sufentanil withdrawal were very similar. Therefore, the evidence was inconclusive as to the contribution of metabolites during withdrawal. / Systemic administration of M3G alone and in combination with morphine produced no withdrawal-like behaviors. However, when these drugs were given centrally, withdrawal-like behaviors were observed in conjunction with seizures. The seizures were not attenuated by naloxone (but were alleviated by an anti-convulsant), indicating that they were not mediated by opioid receptors. The behaviors resembled those seen by previous investigators following high doses of morphine. The results suggest that M3G may play a role in the toxic effects of high doses of morphine.

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The present study investigated the neural mechanisms by which environmental stimuli guide conditioned behaviors in the amphetamine conditioned place preference (CPP) paradigm. Systemically injected D1 and D2 dopamine antagonists blocked both acquisition and expression of the CPP: the selective D1 antagonist more effectively blocked expression than the D2 antagonists. The site of action of the antagonists on expression was the nucleus accumbens. Systemically injected reserpine, but not intra-accumbens a-MPT microinjections, also blocked the expression of the amphetamine CPP. Pre-conditioning and post-conditioning electrolytic or excitotoxic lesions of the lateral amygdaloid nucleus impaired the CPP. It was concluded that the effect of conditioned incentive stimuli is mediated by a neural system which involves the reserpine-sensitive dopamine pool and the D1 dopamine receptor in the nucleus accumbens and the lateral amygdaloid nucleus.