A motivational system approach to avoidance behavior is presented. According to this approach, a motivational state increases the probability of relevant response patterns and establishes the appropriate or “ideal” consummatory stimuli as positive reinforcers. In the case of feeding motivation, for example, hungry rats are likely to explore and gnaw, and to learn to persist in activities correlated with the reception of consummatory stimuli produced by ingestion of palatable substances. In the case of defense motivation, fearful rats are likely to (...) flee or freeze, and to learn to persist in activities correlated with consummatory stimuli produced by flight from a dangerous place. Defense system activation is distinct from alarm reactions. The latter prepare the animal for probable noxious events, involve relatively intense negative affect and extinguish rapidly in situations where the noxious event no longer occurs. In contrast, defense system activation potentiates innate and modified defense reactions, thus preparing the animal for possible, but not necessarily probable, noxious events; it involves little or no negative affect and extinguishes very slowly when the noxious event no longer occurs. With these assumptions and the resulting model we attempt to resolve several long-standing problems in avoidance learning, including the low correlation between negative affect and avoidance performance, differential rates of extinction for avoidance performance and conditioned emotional responses, and evidence that some avoidance responses are much more easily learned than others. In addition, the model has implications for the study of parallels between appetitive and aversive motivation, sign tracking in aversive conditioning, and orientation of flight responses. Historical antecedents and alternative approaches are discussed. (shrink)

Animal research suggests that central serotonergic neurons are involved in behavioral suppression, particularly anxiety-related inhibition. The hypothesis linking decreased serotonin transmission to reduced anxiety as the mechanism in the anxiolytic activity of benzodiazepines conflicts with most clinical observations. Serotonin antagonists show no marked capacity to alleviate anxiety. On the other hand, clinical signs of reduced serotonergic transmission (low 5-HIAA levels in the cerebrospinal fluid) are frequently associated with aggressiveness, suicide attempts, and increased anxiety. The target article attempts to reconcile such (...) human and animal findings by investigating whether anxiety reduction or increased impulsivity is more Likely to account for animal behavioral changes associated with decreased serotonergic transmission. The effects of manipulating central serotonin in experimental anxiety paradigms in animals (punishment, extinction, novelty) are reviewed and compared with the effects of antianxiety drugs. Anxiety seems neither necessary nor sufficient to induce control by serotonergic neurons on behavior. Further evidence suggests that behavioral effects of anxiolytics thought to be mediated by decreases in anxiety are not caused by the ability of these drugs to reduce serotonin transmission. Blockade of serotonin transmission, especially at the level of the substantia nigra, results in a shift of behavior toward facilitation of responding. This behavioral shift is particularly marked when there is competition between acting and restraining response tendencies and when obstacles prevent the immediate attainment of an anticipated reward. It is proposed that serotonergic neurons are involved not only in behavioral arousal but also in enabling the organism to arrange or tolerate delay before acting. Decreases in serotonin transmission seem to be associated with the increased performance of behaviors that are usually suppressed, though not necessarily because of the alleviation of anxiety, which might contribute to the suppression. (shrink)

This paper proposes that human expression of pain in the presence or absence of caregivers, and the detection of pain by observers, arises from evolved propensities. The function of pain is to demand attention and prioritise escape, recovery, and healing; where others can help achieve these goals, effective communication of pain is required. Evidence is reviewed of a distinct and specific facial expression of pain from infancy to old age, consistent across stimuli, and recognizable as pain by observers. Voluntary control (...) over amplitude is incomplete, and observers can better detect pain that the individual attempts to suppress rather than amplify or simulate. In many clinical and experimental settings, the facial expression of pain is incorporated with verbal and nonverbal vocal activity, posture, and movement in an overall category of pain behaviour. This is assumed by clinicians to be under operant control of social contingencies such as sympathy, caregiving, and practical help; thus, strong facial expression is presumed to constitute an attempt to manipulate these contingencies by amplification of the normal expression. Operant formulations support skepticism about the presence or extent of pain, judgments of malingering, and sometimes the withholding of caregiving and help. To the extent that pain expression is influenced by environmental contingencies, however, could equally plausibly constitute the release of suppression according to evolved contingent propensities that guide behaviour. Pain has been largely neglected in the evolutionary literature and the literature on expression of emotion, but an evolutionary account can generate improved assessment of pain and reactions to it. (shrink)

The past 50 years have seen an accumulation of evidence suggesting that associative learning depends on high-level cognitive processes that give rise to propositional knowledge. Yet, many learning theorists maintain a belief in a learning mechanism in which links between mental representations are formed automatically. We characterize and highlight the differences between the propositional and link approaches, and review the relevant empirical evidence. We conclude that learning is the consequence of propositional reasoning processes that cooperate with the unconscious processes involved (...) in memory retrieval and perception. We argue that this new conceptual framework allows many of the important recent advances in associative learning research to be retained, but recast in a model that provides a firmer foundation for both immediate application and future research. (shrink)