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Classical conditioning occurs when neutral stimuli are associated with a psychologically significant event. The main result is that the stimuli come to evoke a set of responses or emotions that may contribute to many clinical disorders, including (but not limited to) anxiety disorders and drug dependence. Research on conditioning has uncovered many surprising details about the underlying learning process, as well as methods for eliminating emotional and behavioral problems.
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1. Historical Background
Classical conditioning was first studied systematically at the turn of the twentieth century by the Russian physiologist, Ivan Pavlov (Pavlov 1927). In the usual description of his best-known experiment, Pavlov rang a bell and then gave a dog some food. After a few pairings of bell and food, the dog began to salivate to the bell, and thus anticipated the presentation of food. The classical conditioning phenomenon quickly attracted psychologists who applied it to clinical issues. Before most of Pavlov’s work was available in English, John Watson showed that human emotions are also influenced by classical conditioning (Watson and Rayner 1920). Watson showed an infant boy a stimulus (which happened to be a laboratory rat) and then made a frightening noise. After a few pairings of the rat and the noise, the child became afraid whenever the rat was presented. This fear generalized to a rabbit, a dog, and a fur coat. Watson saw conditioning as a means by which emotions could be elicited by an expanding range of cues.
The application of conditioning to clinical issues became central to the behavior therapy movement that began in the 1950s and 1960s (e.g., Wolpe 1958). The idea was that psychiatric disorders could be understood and treated using scientifically established principles of learning. The view that anxiety disorders result from classical conditioning was later criticized (e.g., Rachman 1977). However, many of the criticisms were directed at an obsolete view of conditioning, the science of which continued to advance after behavior therapy began (see below).
2. Behavioral Consequences Of Classical Conditioning
The events in Pavlov’s experiment are often described using terms designed to make the experiment applicable to any situation. The food is the ‘unconditional stimulus,’ or US, because it unconditionally elicits salivation before the experiment begins. The bell is known as the ‘conditional stimulus,’ or CS, because it only elicits the salivary response conditional on the bell–food pairings. The new response to the bell is correspondingly called the ‘conditional response’ (CR), while the natural response to the food itself is the ‘unconditional response’ (UR).
Culture has created the impression that conditioning is a rigid affair in which a fixed event comes to elicit a fixed response. In fact, conditioning is more complex and dynamic than that. For example, signals for food may evoke a large set of responses that prepare the organism to digest food: They can elicit secretion of gastric acid, pancreatic enzymes, and insulin in addition to the famous salivary response. The CS can also elicit approach behavior, an increase in body temperature, and a state of arousal and excitement. When a signal for food is presented to a quiescent, food-replete animal, the animal may get up and eat more food. Signals for food evoke a whole ‘behavior system’ that is functionally organized to deal with the meal (Timberlake 1994).
Classical conditioning is also involved in other aspects of eating. Through conditioning, humans may learn to like or dislike different foods. In infrahuman animals, flavors associated with nutrients (sugars, starches, calories, proteins, or fats) come to be preferred. Flavors associated with sweet tastes are also preferred, while flavors associated with bitter tastes are avoided. At least as important, flavors associated with illness become disliked, as illustrated by the person who gets sick drinking tequila and consequently learns to hate the flavor. The fact that flavor CSs can be associated with such a range of biological consequences (USs) is important for omnivorous animals that need to learn about new foods. And it has clinical implications. For example, chemotherapy can make cancer patients sick, and can therefore cause the conditioning of an aversion to a food that was eaten recently (or to the clinic itself). And conditioning can enable external cues to trigger food consumption and craving, a potential influence on overeating and obesity.
Classical conditioning also occurs when we ingest drugs. Whenever a drug is taken, it constitutes a US, and it may be associated with potential CSs that are present at the time (rooms, odors, injection rituals, etc.). CSs that are associated with drug USs can have an interesting property: They often elicit a conditioned response that seems opposite to the unconditional effect of the drug (Siegel 1989). For example, although morphine causes a rat to feel less pain, a CS associated with morphine elicits an opposite increase, not a decrease, in pain sensitivity. Similarly, although alcohol can cause a drop in body temperature, a conditioned response to a CS associated with alcohol is typically an increase in body temperature. In these cases, the conditioned response is said to be ‘compensatory’ because it counteracts the drug effect. Compensatory responses are another example of how classical conditioning helps organisms prepare for a biologically significant US.
Compensatory conditioned responses have implications for drug abuse. First, they can cause drug tolerance, in which repeated administration of a drug reduces its effectiveness. As a drug and a CS are repeatedly paired, the compensatory response to the CS becomes stronger and more effective at counteracting the effect of the drug. The drug therefore has less impact. One implication is that tolerance will be lost if the drug is taken without being signaled by the usual CS. Consistent with this idea, administering a drug in a new environment can cause a loss of drug tolerance and make drug overdose more likely (see Siegel 1989). A second implication stems from the fact that compensatory responses may be unpleasant. A CS associated with an opiate may elicit several compensatory responses—it may cause the drug user to be more sensitive to pain, undergo a change in body temperature, and perhaps become hyperactive (the opposite of another unconditional morphine effect). The unpleasantness of these responses may motivate the user to take the drug again to get rid of them. Compensatory responses may often resemble withdrawal effects (Siegel 1989). The idea is that the urge to take drugs may be strongest in the presence of CSs that have been associated with the drug. The hypothesis is consistent with self-reports of abusers who, after a period of abstinence, are tempted to take the drug again when they are re-exposed to drug-associated cues.
Classical conditioning is also involved in anxiety disorders, as Watson originally envisioned. We now know that CSs associated with frightening USs can elicit a whole system of conditioned fear responses, again broadly designed to help the organism cope. In animals, cues associated with frightening events elicit a set of natural defensive reactions that have evolved to prevent attack by predators. They also elicit changes in respiration, heart rate, and blood pressure, and even a (compensatory) decrease in sensitivity to pain. Brief CSs that occur close to the US in time can also elicit adaptively timed protective reflexes. For example, the rabbit blinks to a brief signal that predicts a mild electric shock near the eye. The same CS, when lengthened in duration and paired with the same US, elicits mainly fear responses. And fear elicited by a CS may potentiate the conditioned eye-blink response elicited by another CS or a startle response to a sudden noise. Once again, CSs do not merely elicit a simple reflex, but evoke a complex and interactive set of responses.
Classical fear conditioning can contribute to phobias (where specific objects may be associated with a traumatic US) as well as other anxiety disorders. For example, in panic disorder, people who have unexpected panic attacks can become anxious about having another one. In this case, the panic attack (the US or UR) may condition anxiety to the external situation in which it occurs (e.g., a crowded bus) and also internal (‘interoceptive’) CSs created by early symptoms of the attack (e.g., dizziness or a sudden pounding of the heart). These CSs may then come to evoke anxiety or panic responses. Panic disorder may begin because external cues associated with panic can arouse anxiety, which may then exacerbate the next unconditional panic attack and or panic response elicited by an interoceptive CS (Bouton et al. 2001). Interestingly, the emotional reactions elicited by CSs may not require conscious awareness for their occurrence or development. Indeed, fear conditioning may be independent of conscious awareness (e.g., LeDoux 1996).
In addition to eliciting conditioned responses, CSs also motivate ongoing behavior. For example, presenting a CS that elicits anxiety can increase the vigor of instrumental or operant behaviors that have been learned to avoid or escape the frightening US. Thus, an individual with panic disorder will be more likely to express avoidance in the presence of anxiety cues. Similar effects may occur with CSs that predict other USs (such as drugs or food)—as already mentioned, a drug-associated CS may motivate the drug abuser to take more drugs. The potential influence of classical conditioning on behavior is thus extensive and ubiquitous.
3. The Learning Process In Classical Conditioning
Modern research has revealed some important details about the learning process that underlies classical conditioning (Rescorla 1988). For example, conditioning is not an inevitable consequence of pairing a CS with a US. Such pairings will not cause conditioning if there is a second CS present that already predicts the US (Kamin 1969). This sort of finding (‘blocking’) suggests that a CS must provide new information about the US if learning is to occur. Many theorists now suppose that conditioning is determined by the discrepancy between (a) the US predicted by all CSs present on a trial and (b) the US that actually happens on the trial (Rescorla and Wagner 1972). One implication is that, depending on the size and direction of the discrepancy, the pairing of a CS and traumatic US, for example, can cause an increase in fear conditioning, no change in conditioning, or even a decrease in conditioning.
The latter implication is interesting. A new CS can acquire a negative value if the US is smaller than that which other CSs present predict. Casually speaking, the new CS predicts ‘less US than expected.’ Such negative signals are called ‘conditioned inhibitors’ because they inhibit performance elicited by other CSs. They are clinically relevant because they may hold pathological CRs like anxiety at bay. A loss of the inhibition would allow the anxiety response to emerge. Classical conditioning is most robust if the CS and US are intense or salient. It is also best if the CS and US are novel. For example, in ‘latent inhibition,’ repeated exposure to the CS alone before conditioning can diminish its ability to elicit responding when it is paired with the US. In the ‘US pre-exposure effect,’ repeated exposure to the US before conditioning can likewise decrease the conditioning that later occurs when a CS and the US are paired. One idea is that the CS and the US must be ‘surprising’ at the time of their pairing for learning to occur. Thus, the effects of pairing a CS with trauma or drug USs may depend in subtle ways on the individual’s prior experience with the CS and US.
There are important variants of classical conditioning. In ‘sensory preconditioning,’ two stimuli (A and B) are first paired, and then one of them (A) is later paired with the US. Stimulus A evokes conditioned responding, of course, but so does stimulus B— indirectly, through its association with A. One implication is that exposure to a potent US like a panic attack may influence our reactions to stimuli that have never been paired with the US directly; the sudden anxiety response to stimulus B might seem spontaneous and mysterious. A related finding is ‘second-order conditioning.’ Here, A is paired with a US first and then subsequently paired with stimulus B. Once again, both A and B will evoke responding. Sensory preconditioning and second-order conditioning in-crease the range of stimuli that can control conditioned responses.
Emotional responses can also be conditioned through observation. For example, a monkey that merely observes another monkey being frightened by a snake can learn to be afraid of the snake itself (Mineka 1992). The observer learns to associate the snake (CS) with its own emotional reaction (US UR) to the other monkey being afraid. Although monkeys readily learn to fear snakes, they are less likely to associate other salient cues (such as colorful flowers) with fear in the same way. This is an example of ‘preparedness’ in classical conditioning—some stimuli are especially effective signals for some USs because evolution has made them that way. (Another example is the fact that tastes are easily associated with illness but not shock, whereas auditory and visual cues are easily associated with shock but not illness.) Preparedness may explain why human phobias tend to be for certain objects (snakes or spiders) and not others (knives or electric sockets) that may as often be paired with pain or trauma.
4. ‘Unlearning’ In Classical Conditioning
Once one accepts a role for conditioning in behavioral and emotional disorders, the question becomes how to eliminate it. Pavlov studied ‘extinction’: conditioned responding decreases if the CS is presented repeatedly without the US after conditioning. Extinction is the basis of many therapies that reduce pathological conditioned responding through repeated exposure to the CS. Another elimination procedure is ‘counterconditioning,’ in which the CS is paired with a very different US UR. Counterconditioning was the inspiration for ‘systematic desensitization,’ a behavior therapy technique in which frightening CSs are deliberately associated with relaxation during therapy (Wolpe 1958).
Although extinction and counterconditioning reduce unwanted conditioned responses, they do not destroy the original learning, which remains in the brain, ready to return to behavior under the right circumstances. For example, conditioned responses that have been eliminated by extinction or counterconditioning can recover if time passes before the CS is presented again (‘spontaneous recovery’). Conditioned responses can also recover if the patient returns to the original context of conditioning (the general situation, mood, or state in which conditioning occurred), or if the current context is associated with the US (Bouton 2000). All of these phenomena are potential mechanisms for relapse. Techniques that may minimize relapse include conducting therapy in the contexts where the disorder is a problem, conducting therapy in multiple contexts, or providing the client with retrieval cues or retrieval strategies that help recall therapy (Bouton 2000). In the long run, contemporary research on extinction and counterconditioning may suggest ways to optimize their clinical effectiveness.
5. Challenges
The idea that classical conditioning is a basis of behavior disorders, particularly anxiety disorders, has not gone unchallenged. However, most challenges have been directed at early versions of conditioning theory that did not recognize factors such as information value, latent inhibition, preparedness, or context. For instance, Rachman (1977) noted that London air raids during World War II did not cause an increase in anxiety disorders despite their emotional impact. We now know that air raids might not have caused conditioning if the potential CSs were familiar rather than novel, if the raids were experienced in the presence of safety cues that inhibited fear (e.g., relatives, bomb shelters), or if the raids were signaled by other cues (e.g., sirens) that could have ‘blocked’ conditioning of potential CSs (Kamin 1969). Another criticism was that fears in the general population are disproportionately directed toward things like snakes, a fact that is consistent with the preparedness principle (above). As a final example, critics of conditioning explanations of panic disorder have asked why a CS like a pounding heart does not elicit panic in the context (say) of athletic exercise, or why extinction exposure to the CS without panic during exercise does not eliminate its ability to cause panic in other situations. The answer may be that the loss of responding that occurs in extinction is especially specific to the context in which it is learned (Bouton et al. 2001). Thus, although fear may extinguish in the context of exercise, that extinction will not abolish the CS’s ability to elicit fear in other contexts, such as a crowded bus or a shopping mall. The fact that conditioned responses generalize more across contexts than extinction does may be a reason why many disorders are so persistent.
6. Future Directions
Basic research on classical conditioning will continue to investigate the circumstances that allow (and prevent) conditioning to occur, how conditioning is represented in memory and the brain, and how it ultimately influences cognitions, emotions, and behavior. Research will also address how extinction and other behavior-elimination procedures work and can be improved. That research may eventually explain why conditioning processes like extinction seem more context-specific than conditioning itself. And it will also eventually provide a more complete account of the factors that determine the nature and form of conditioned responses, and how the many responses that CSs can evoke can also interact and interrelate.
As our understanding of classical conditioning continues to deepen and expand, so will our insight into its possible role in various clinical disorders. Understanding the role of conditioning in causing a disorder, however, will probably also require prospective studies in which clinical investigators observe conditioning trials as they naturally occur in the world and then measure their effects as the disorder actually develops. It will also benefit from a better appreciation of how conditioning processes interact with biological factors (such as genetically linked vulnerabilities) that may also play a role. And it will benefit from a better understanding of how conditioning interacts with cognitive factors such as thoughts, beliefs, and awareness. Although biological and cognitive factors are sometimes viewed as alternatives to simple learning processes like classical and operant conditioning, a complete appreciation of any disorder will probably require a more integrative perspective on how these factors work in combination.
In the meantime, classical conditioning remains a surprisingly rich scientific phenomenon that can be expected to come into play whenever people experience significant emotional and biological events and can associate them with other events in their world.
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