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Endothelial cells from rat brain microvessels, human aortic artery and human umbilical vein were examined, together with ex vivo rat brain capillaries and rat aortic ring sections, for the expression of opioid receptor-like OP-4 mRNA and protein. High levels of mRNA expression and an immunopositive reaction for the receptor protein were detected in the endothelial cells from primary and from established in vitro cultures, as well as in the intima of ex vivo rat aortic rings, where the signal was limited to the endothelial layer. Interaction of the OP4 receptor with its physiological ligand nociceptin caused, in cultured endothelial cells, the activation of a mitogen-activated protein (MAP) kinase cascade. Taken together, these results show that the OP4 receptor is synthesised and functionally expressed in endothelial cells, presumably as a starting point for some vasoactive mechanism(s).

The aim of the study was to measure the changes in cerebral energy metabolism and c-fos mRNA expression following challenge with heroin in drug-naive rats and in animals previously sensitized to the drug. Acute heroin administration to drug naive-rats produced a generalized metabolic depression. In contrast, challenge with heroin in drug-sensitized rats produced selective metabolic increases in structures belonging to the basal ganglia. These changes were accompanied by increased c-fos mRNA expression in the caudate-putamen nucleus. These results demonstrate that the process of sensitization to heroin is coupled to functional changes that are confined to the subcortical motor circuits of the basal ganglia.

The [14C]2-deoxyglucose method was applied to measure the effects of the acute intravenous administration of morphine sulphate (0.2–0.4 mg/kg) on cerebral glucose utilization in rats. Morphine produced dose-dependent increases of glucose metabolism in the shell of the nucleus accumbens, without affecting functional activity in any other brain area. These results provide further evidence for the preferential effects of intravenously abused substances in the shell of the nucleus accumbens.

The serotonin (5-HT) agonists, D-lysergic acid diethylamide (LSD) and 5-methoxytryptamine (5-Me-O-T), dose dependently inhibited the K+-evoked outflow of [3H]5-HT from preloaded rat hippocampal slices in vitro, indicating activation of the 5-HT autoreceptor. However, this effect was abolished in slices pretreated with pertussis toxin. It is thus concluded that the 5-HT autoreceptor in the hippocampus is coupled to G proteins.