Context dependency of conditioned aversions to water and sweet tastes.

Three experiments exposed rats (Rattus norvegicus) to a discriminative conditioning procedure whereby a specific fluid was followed by lithium in one environment but not in another. This produced context-specific aversion to water, as detected by 2-bottle tests in Experiment 1, and a context-dependent saccharin aversion, which was unaffected by context extinction, in Experiment 2. Experiment 3 found that sucrose preexposure increased contextual control over the aversion established by sucrose-lithium pairings but had no effect on the target context. By contrast, target context exposure during conditioning reduced aversion to this context but did not affect contextual control of the sucrose aversion. In conclusion, depending on the conditioning procedures, contextual control of a taste aversion can be independent of the context's Pavlovian properties.

Extinction of within-event learning is contextually controlled and subject to renewal.

Five experiments examined within-event learning in rats by inducing an appetite for one of the elements (salt) of a compound stimulus and assessing preference for the other element (almond). Almond preference was conditional upon (1) the almond flavour having been presented in compound with the salt, and (2) the assessment being conducted when the rats were out of sodium balance (Experiment 1). Presentations of the compound in one environment (A) and of the salt and almond elements in a second environment (B) resulted in greater almond preference when rats were tested in A than in B (Experiment 2). Almond preference was reduced when separate presentations of the compound and almond (Experiment 3) or of the compound and salt (Experiment 4) occurred in the same environments but not when these presentations occurred in different environments. Rats exposed to the compound in A and then extinguished to the elements in either A or B showed a reduced almond preference when tested in the extinction environment, but not when tested in the other environment (Experiment 5). Thus, extinction of within-event learning is context-specific and subject to renewal. The results were interpreted in terms of an associative model whereby separate presentations of the elements result in a symmetrical inhibitory link which is contextually gated (Bouton, 1993).

Effects of morphine and naloxone upon the reactions of rats to a heat stressor.

Five experiments used rats to examine the conditioned hypoalgesia induced by exposure to a heated floor. Experiments 1 and 2 demonstrated that this hypoalgesia is mediated by non-opioid mechanisms of pain control, as evidenced by insensitivity to the opioid antagonist naloxone and by the absence of cross-tolerance with the opioid agonist morphine. Although non-opioid in nature, the acquisition of conditioned hypoalgesia was facilitated by naloxone and impaired by morphine (Experiments 3 and 4). These effects did not appear to be due to an opioid regulation of pain. (1) Pairing morphine with the heated floor attenuated acquisition in drug-tolerant rats. (2) This attenuation by morphine was removed when naloxone was given after exposure to the heated floor. (3) Conditioning was facilitated when naloxone was given after exposure to the heated floor (Experiment 5). The results were discussed in terms of an opioid regulation of (a) surprise, (b) arousal of an aversive motivational system, and (c) the affective component of pain.

Aversive conditioning in the rat: effects of a benzodiazepine and of an opioid agonist and antagonist on conditioned hypoalgesia and fear.

Hypoalgesia and fear co-occurred in rats trained on a heated floor and tested for their latencies to paw lick on that floor and to step down onto a nonheated floor. These responses were extinguished, suggesting a mediation by aversive conditioning processes. A benzodiazepine impaired the acquisition of aversive conditioning, but it did not attenuate the expression of conditioned hypoalgesia. The opioid agonist morphine also impaired acquisition across a range of drug doses and variations in hypoalgesic tolerance, whereas the opioid antagonist naloxone facilitated acquisition. The results are discussed in terms of the perceptual-defensive-recuperative (Fanselow, 1986) and working memory (Grau, 1987) models of the mechanisms for the co-occurrence of conditioned hypoalgesia and fear.