Search

This study evaluated whether the intensity of previously smelled odors could unintentionally influence the subsequent judgement of odor intensity. The predicted context effect was based on the adaptation-level theory. Before and 25 min after either WEAK or STRONG biasing odor concentrations, 51 subjects were required to rate the intensity of 10 different odor concentrations of California Orange Oil. After the WEAK bias, subjects judged the odor intensity as being stronger than they did after the STRONG bias. Thus the intensity of odors smelled 25 min earlier can unintentionally influence subsequent odor intensity judgement. The findings are discussed in the light of two alternative explanations, namely, a central implicit memory process and a stimulus-level-based change at the peripheral level.

There is evidence for neurodevelopment disturbances in schizophrenia. In rats, a neonatal basolateral amygdala lesion induces behavioural features in adults reminiscent of the symptomatology of schizophrenia. Dopamine plays a key role in the pathogenesis of schizophrenia, and cannabis use has been implicated in the risk for developing schizophrenia. The effects of an excitotoxic, bilateral basolateral amygdala lesion on postnatal days 7 or 21 were compared when the rats were adult. The behavioural response to a novelty challenge and the level of dopamine receptors and cannabinoid receptors in the brain using in-vitro autoradiography was determined. In brain tissue punches concentrations of monoamines and metabolites were determined by high-performance liquid chromatography. The neonatal lesion, but not the later lesion induced behavioural hyperactivity and biochemical effects. The neonatal lesion reduced the density of dopamine D 2 -like, but not D 3 -, and less markely D 1 -like receptors and increased dopamine turnover. These effects were observed in the mesolimbic, but not in the striatal regions. In contrast, density of cannabinoid receptors was increased in the striatal, but not the mesolimbic regions of these animals. Noradrenergic neurotransmission was reduced in both regions. The present findings contribute to the idea that the neonatal basolateral amygdala lesion induces features in adults reminiscent of the neurodevelopmental disturbances in schizophrenia, with a focus on the amygdalaprefrontal cortex-nucleus accumbens circuit.

The functional recovery from impaired motor activity induced by 6-hydroxydopamine lesions in rat nucleus accumbens was accelerated by subcutaneous treatment with the ACTH-(4–9) analogue Met/O2/-Glu-His-Phe-D-Lys-Phe (ORG 2766). Treatment was effective after daily injections of ORG 2766 dissolved in saline during the first 6 days following the lesion (ED50: 28.5 ng kg−1 day−1) or after a single injection of the peptide in a biodegradable microsphere formulation administered after the lesion (ED50:8.9 ng kg−1 day−1). This study shows that a single injection of a microsphere preparation can replace multiple injections with ORG 2766 in order to facilitate functional recovery after brain damage.

This study concerns the effect of spontaneous acquisition of alcohol drinking in rhesus monkeys on plasma levels of β-endorphin, ACTH, prolactin, cortisol and testosterone. Twelve monkeys had free-choice access to water and two ethanol/water solutions (1%, 2%, v/v) for 4 weeks. During the first 2 weeks, six monkeys were injected (i.m.) twice daily with 0.50 μg/ kg desglycinamide-(Arg8)-vasopressin (DGAVP), a neuropeptide, that has been postulated to interfere with central positive reinforcement processes. The other six were treated with a placebo. Hormonal plasma levels after the first 2 weeks and after another 2 weeks of alcohol drinking were compared to pre-alcohol hormonal levels (baseline). The placebo-treated subjects significantly increased, but the DGAVP-treated subjects significantly decreased ethanol intake over time. After 2 weeks of alcohol, significant increases were found in β-endorphin and ACTH levels. After 4 weeks, prolactin was increased, cortisol decreased and particularly β-endorphin remained significantly increased. No relationship was found between baseline hormonal levels and subsequent ethanol intake. No significant differences in plasma hormonal changes were observed between DGAVP- and placebo-treated subjects. Two placebo-treated subjects that showed the highest increase in ethanol intake over time, reacted differently, by reducing β-endorphin and ACTH levels over time, showing the largest decreases in cortisol and hardly any prolactin reaction. It is concluded that spontaneous alcohol drinking by naive subjects disturbs hormonal processes and that two animals deviated with respect to the acquisition in alcohol drinking and endocrine functioning.

The alcohol supply (a 16% and a 32%, v/v, ethanol-in-water solution) for eight male rhesus monkeys, who already have had free access to water and ethanol solutions concurrently for about one year, was interrupted for 1, 2 or 7 days. The previously acquired ethanol consuming behaviour appeared very resistant to extinction, because ethanol consumption was immediately resumed after renewed access, even at a temporarily increased level. Since physical withdrawal distress was not observed and the increase was higher when interruption lasted longer, the observed behaviour could be attributed to the reinforcing effects of ethanol, leading to specific ethanol-directed behaviour.

The influence of sublingually administered desglycinamide9-arginine8-vasopressin (DGAVP) on ambulant methadone-detoxification of heroin addicts was investigated in two double blind, placebo controlled trials. It was found that treatment with DGAVP during the initial phase of methadone-detoxification of mild to moderate heroin addicts facilitated detoxification. These results and animal data concerning the interaction of DGAVP with heroin self-administration suggest that DGAVP may reduce the reinforcing action of heroin. DGAVP may have a similar effect on the action of cocaine, because the use of this latter drug by the addicts was also decreased by the peptide treatment.

A common denominator for the occurrence of abuse with various drugs is their reinforcing action, which can be analysed reliably in experimental animals by drug self-administration. This behaviour is influenced by external factors, drug-induced alterations of homeostatic mechanisms in the body and by internal factors. These internal factors are directly related to reinforcement or could modulate the drug-induced reinforcing activity. Experimental data show that the opioid peptide β-endorphin acts as a positive reinforcer in rats and that desglycinamide9 -arginine8 -vasopressin decreases acquisition of heroin self-administration in these animals. It is concluded that brain neuropeptide systems are operative in the reward mechanism and may be implicated in the acquisition of drug seeking behaviour; this may be of relevance to the underlying mechanisms of drug addiction.