Search

To examine the hypothesis that Pavlovian autoshaping provides an animal learning model of drug abuse, two studies evaluated the induction of ethanol drinking by autoshaping procedures. In Experiment 1, the sipper tube conditioned stimulus (C S) contained saccharin/ethanol solution and was repeatedly paired with food as an unconditioned stimulus (US). The CS-US paired group consumed more of the 0.1% saccharin-6% ethanol solution than did the CS-US random group, revealing that autoshaping conditioned responses (CR) induce ethanol drinking not attributable to pseudo-conditioning. Experiment 2 employed saccharin-fading procedur es and showed that the paired vs random group differences in ethanol drinking were maintained, even as the saccharin was eliminate d from the solution. The results show that Pavlovian autoshaping procedures induce high volumes of ethanol drinking when the pres enta- tion of a sipper tube containing an ethanol solution precedes the response-independent delivery of food. The high volume of eth anol consumed in a brief period of time suggests that Pavlovian autoshaping may be a model of binge drinking.

Research on the interaction of ethanol (ET) and stress published since 1981 is reviewed. Chronic physical stressors were found to increase the ingestion of ET compared to nonstressed animals. With foodshock, ingestion of ET decreased during the stress session but rose afterwards. The elevation of ET ingestion produced by daily immobilization was long-lasting and was related to individual initial preference for ET. Psychological stressors also increased ingestion of ET. In rat colonies, dominant rats ingested less ET, whereas submissive rats had the highest intake. Factors that modify the ingestion of ET include neonatal experience and REM sleep deprivation. Early weaning increased, while postnatal handling decreased preference for ET. The effect of postnatal handling may be influenced by genetics. Stress, applied during adult life or prenatally, modifies some, but not all, the acute effects of ET. There were marked individual differences in the interaction of ET and stress with respect to ingestion of ET. Conversely, ET may modify stress-induced behavioural and neurochemical changes. This interaction may be stressor specific. Some stressors increase the ET's effects, whereas others may decrease or not affect them. In brain, ET has been shown to lessen the stress-induced decrease in noradrenaline and 5-hydroxytryptamine (serotonin) levels and those in noradrenaline turnover and alpha 1-receptor binding. Stress-induced changes in plasma catecholamines, corticosterone, non-esterified fatty acids and amino acids, and in the decline in adrenal catecholamines are also lessened by pretreatment with ET. Possible mechanisms for the ET-stress interaction are discussed. These include mediation via the GABA-benzodiazepine-ionophore complex, endogenous opioids, the hypothalamo-pituitary-adrenocortical axis and the noradrenergic system.