In this article I review research and theory on the "interference paradigms" in Pavlovian learning. In these situations (e.g., extinction, counterconditioning, and latent inhibition), a conditioned stimulus (CS) is associated with different unconditioned stimuli (USs) or outcomes in different phases of the experiment; retroactive interference, proactive interference, or both are often observed. In all of the paradigms, contextual stimuli influence performance, and when information is available, so does the passage of time. Memories of both phases are retained, and performance may depend on which is retrieved. Despite the similarity of the paradigms, conditioning theories tend to explain them with separate mechanisms. They also do not provide an adequate account of the context's role, fail to predict the effects of time, and overemphasize the role of learning or storage deficits. By accepting 4 propositions about animal memory (i.e., contextual stimuli guide retrieval, time is a context, different memories are differentially dependent on context, and interference occurs at performance output), a memory retrieval framework can provide an integrated account of context, time, and performance in the various paradigms.

Context, time, and memory retrieval in the interference paradigms of Pavlovian learning.

How the brain codes, stores, and retrieves memories is among the most important and baffling questions in science. The uniqueness of each human being is due largely to the memory store—the biological residue of memory from a lifetime of experience. The cellular basis of this ability to learn can be traced to simpler organisms. In the past generation, understanding of the biological basis of learning and memory has undergone a revolution. It is clear that various forms and aspects of learning and memory involve particular systems, networks, and circuits in the brain, and it now appears possible to identify these circuits, localize the sites of memory storage, and analyze the cellular and molecular mechanisms of memory.

Learning and memory

Excessive fear and anxiety are hallmarks of a variety of disabling anxiety disorders that affect millions of people throughout the world. Hence, a greater understanding of the brain mechanisms involved in the inhibition of fear and anxiety is attracting increasing interest in the research community. In the laboratory, fear inhibition most often is studied through a procedure in which a previously fear conditioned organism is exposed to a fear-eliciting cue in the absence of any aversive event. This procedure results in a decline in conditioned fear responses that is attributed to a process called fear extinction. Extensive empirical work by behavioral psychologists has revealed basic behavioral characteristics of extinction, and theoretical accounts have emphasized extinction as a form of inhibitory learning as opposed to an erasure of acquired fear. Guided by this work, neuroscientists have begun to dissect the neural mechanisms involved, including the regions in which extinction-related plasticity occurs and the cellular and molecular processes that are engaged. The present paper will cover behavioral, theoretical and neurobiological work, and will conclude with a discussion of clinical implications.

Mechanisms of fear extinction

Because causal relations are neither observable nor deducible, they must be induced from observable events. The 2 dominant approaches to the psychology of causal induction—the covariation approach and the causal power approach—are each crippled by fundamental problems. This article proposes an integration of these approaches thai overcomes these problems. The proposal is that reasoners innately treat the relation between covariation (a function denned in terms of observable events) and causal power (an unobservable entity) as that between scientists' law or model and their theory explaining the model. This solution is formalized in the power PC theory, a causal power theory of the probabilistic contrast model (P. W. Cheng & L. R. Novick, 1990). The article reviews diverse old and new empirical tests discriminating this theory from previous models, none of which is justified by a theory. The results uniquely support the power PC theory.

From covariation to causation: A causal power theory.

Behavioral and Neural Analysis of Extinction

Rats were used in a conditioned-suppression paradigm to investigate why a conditioned inhibition (CS-) does not extinguish when presented alone. Experiment 1 assessed the role of blocking by excitatory contextual cues and/or an evoked representation of the conditioned excitor (CS+), which had been nonreinforced in compound with the CS-. When the CS+ and context were extinguished prior to presentations of the CS- alone, the CS- showed a retardation effect, evidently reflecting latent inhibition, because no inhibition was detected in controls for which presentations of the CS- alone had been omitted. Experiment 2 showed that the loss of conditioned inhibition (CI) was due to excitatory extinction and not to time since conditioning. Furthermore, when excitation was reconditioned to the extinguished CS+ (Experiment 1), or to a novel CS in the same context (Experiment 2), CI was restored. Two other experiments evaluated whether the maintenance of CI depended upon excitation that was generic in form or associatively tied to the training context. They showed no loss of CI when groups received CS+ extinction in that context, along with concomitant presentations in a different context of the US by itself, for a novel CS, or correlated either positively or negatively with the original CS+. Collectively, the findings argue that CI is a "slave" to excitation, for when excitation is extinguished, CI is deactivated; and yet when excitation is reconditioned to the original or a new CS+ in the same or a different context, CI is restored.

Inhibition as a "slave" process: deactivation of conditioned inhibition through extinction of conditioned excitation.

Shock-induced modulation of lymphocyte reactivity: suppression, habituation, and recovery.

Pavlovian conditioning of shock-induced suppression of lymphocyte reactivity: Acquisition, extinction, and preexposure effects.

1. 1. Although bipolar disorder constitutes a major public health problem, with a high risk of suicide and an economic cost exceeding that of unipolar depression, it has received comparatively little attention, particularly at the basic science level. Perhaps as a result of this neglect, there is currently no animal model able to simulate the cyclicity which is its defining characteristic. 2. 2. Consequently, drug development in this area is meager and has proceeded serendipitously rather than empirically. 3. 3. The authors have recently reported that repeated exposure to cocaine and other Stressors can induce an oscillation or cycling in a host of neurochemical and physiological systems. 4. 4. In order to test whether such cycling might be of potential relevance to bipolar disorder, the authors examined whether cocaine-induced cyclicity of amphetamine-evoked efflux of dopamine from slices of rat nucleus accumbens and striatum and/or cocaine induced oscillation of a behavior, stress-induced hypoalgesia, could be prevented by lithium, the agent of choice in treating this disease. 5. 5. The authors report that prophylactic treatment with lithium, completely and specifically prevented oscillations in each instance. This may represent an important initial step toward the development of the first cycling model of bipolar disorder.

The effects of lithium on a potential cycling model of bipolar disorder

Publisher Summary This chapter discusses nature of exploration, its relation to early motivational interpretations, and the manner in which these interpretations may be successfully accommodated within a drive and incentive-motivational theory. The concept of an exploratory drive obtains tentative operational expression in the length and constancy of the animal's exposure to an impinging stimulus condition, or conversely, with the animal's “deprivation” of a change in stimulation. Correspondingly, the magnitude of the incentive or reinforcement involved in the learning of instrumental behaviors may be related to the magnitude of the change in stimulation that is provided by the relatively novel or unfamiliar stimuli to and for which the animal responds. The problem of delineating exploratory phenomena might be viewed with respect to a resolution on the basis of a presumed effect of exploration, that is, the commonly held position that exploratory behaviors have the prime function of altering those stimuli currently impinging upon the organism. Thus, exploration as a label may be relegated to those behaviors that are instrumental to the animal's receipt of relatively novel or changed stimuli.

Harry Fowler

Papers

Inhibition as a "slave" process: deactivation of conditioned inhibition through extinction of conditioned excitation.

Shock-induced modulation of lymphocyte reactivity: suppression, habituation, and recovery.

Pavlovian conditioning of shock-induced suppression of lymphocyte reactivity: Acquisition, extinction, and preexposure effects.

The effects of lithium on a potential cycling model of bipolar disorder

Satiation and Curiosity: Constructs for a Drive and Incentive-Motivational Theory of Exploration1