Learning Theory: Classical Conditioning

Classical (or respondent) conditioning depends on innately evocative stimuli (US) producing an unconditional, reflexive response (UR), such as when physical injury reflexively produces a pain grimace. When a neutral stimulus is paired with the US, the neutral stimulus becomes a conditional stimulus (CS) with powers to elicit a CR that resembles the original UR (Pavlov, 1927). For example, in the case of persons undergoing chemotherapy (US) that causes them to vomit (UR), the nurse may become a CS by association with administration of the chemotherapy. Consequently, sight of the nurse may produce conditional nausea in the patient even before the chemotherapy is administered the next time. Furthermore, through a process of generalization, the CR may begin to emerge in reaction to stimuli similar to the original CS. Following from the preceding example, generalization may result in conditional nausea in response to seeing the medical clinic or administrative staff. In addition, Pavlov (1927) demonstrated that if the CS is presented enough times without the US, the CR lessens or extinguishes. Continuing the example, once the chemotherapy course has completed, repeated visits to the clinic for checkups would result in an eventual diminution of the conditional nausea response.

The principles of aversive classical conditioning are applied mostly to anxiety disorders. Early theorizing of fears and phobias relied on contiguous classical conditioning models in which a neutral stimulus develops conditional fear-provoking properties simply by virtue of close temporal pairing with an aversive stimulus. Examples would include ridicule and rejection by a peer group leading to conditional fear (i.e., phobia) of social situations or barking by a ferocious dog leading to phobias of dogs. These early theories were criticized for being too simplistic (e.g., Rachman, 1978), especially as not everyone who undergoes an aversive experience develops a phobia. That is, not everyone who is ridiculed by a peer group develops social phobia, and not everyone who is barked at by a ferocious dog develops a phobia of dogs. Recent revisions to classical conditioning models of fear and anxiety (see Mineka & Zinbarg, 2006, for a review) correct the earlier pitfalls.

The newer models continue to emphasize the role of aversive experiences in the formation of conditional anxiety responses, but instead of being limited to direct experience with negative events, they extend to conditioning through vicarious observation of negative events or even informational transmission about negative events (see Mineka & Zinbarg, 2006, for citations of supportive research). For example, observing someone else be physically injured and/or be terrified in a car accident maybe sufficient for the development of a conditional fear of motor vehicles, as would being told about the dangers of driving and the high likelihood of fatal car accidents. Vicarious and informational transmission of conditioning represents the incorporation of cognitive processes into classical conditioning models. The newer conditioning models also recognize that a myriad of constitutional, contextual, and post-event factors moderate the likelihood of developing a conditional phobia after an aversive event. Constitutional factors (or individual difference variables) include temperament. For example, individuals who tend to be more nervous in general are believed to be more likely to develop a conditional phobia after a negative experience than less “neurotic” individuals who undergo the same negative experience. Another constitutional factor is personal history of experience with the stimulus that is subsequently paired with an aversive event, as prior positive experience may buffer against the development of a conditional phobia. For example, the effects of observing one parent react fearfully to heights may be buffered by having previously observed other family members react without fear to heights. Recognition of individual difference factors addresses the earlier criticism that not everyone who undergoes an aversive experience develops a phobia; rather, certain individuals are prone to developing conditional phobic responses following an aversive experience as a function of their temperament and life experience.

Contextual factors at the time of the aversive experience include intensity and controllability: More intense and less controllable negative events are more likely to generate conditional fear than less intense and/or more controllable negative events. According to these premises, individuals trapped for a lengthy period of time inside an elevator stuck between floors would be more likely to develop a conditional fear of elevators than the person who can escape from a stuck elevator relatively quickly. Similarly, soldiers at the front line of combat would be more likely to develop conditional fear than those further away. Another contextual factor pertains to principles of preparedness, or the innate propensity to rapidly acquire conditional fear of stimuli that posed threat to our early ancestors (Seligman, 1971). Examples of such stimuli are heights, closed-in spaces from which it is difficult to escape, reptiles, and signals of rejection from one’s group. Thus, as a species, humans are more likely to develop long-lasting conditional fears following negative experiences in prepared situations (e.g., being laughed at by peers) compared to other, “nonprepared” situations (e.g., being shocked by an electric outlet). Preparedness is believed to account for the nonrandomness of phobias, or the fact that some objects or situations are much more likely to become feared than other objects.

Following conditioning, a variety of postevent processes may influence the persistence of conditional fear, including additional aversive experiences, expectancies for aversive outcomes (Davey, 2006), and avoidant responding. For example, the child who is teased by a peer group, then ruminates about being teased, expects further teasing, and avoids the peer group is more likely to develop social anxiety than the child who undergoes the same teasing but returns to the peer group the next day. In sum, recent models of classical conditioning recognize that the development of an excessive and chronic conditional fear is not explained by a specific aversive event in isolation but by an interaction among predisposing features, the aversive event, and reactions to the event.

The classical conditioning model is also applicable to disorders related to substance use, in which the principles of appetitive conditioning apply as well as aversive conditioning. Appetitive conditioning refers to conditioning with a US that produces an innately positive response, whereas aversive conditioning refers to conditioning with a US that produces an innately negative response. In the case of substance use disorders, euphoria serves as an innately positive UR to the drug. Over time, environmental stimuli present during the euphoric state become conditional. These environmental stimuli may be the locations in which the drugs are usually consumed or the people with whom drug taking normally occurs. Consequently, the environmental stimuli elicit conditional urges or cravings to take more of the drug. Known as the conditioned appetitive motivational model of craving (Stewart, deWit, & Eikelboom, 1984), this model explains the difficulties experienced when recovering drug users return to the environments in which they originally developed their drug dependence. That is, just seeing a group of friends with whom drugs used to be taken may be enough to produce cravings for the drugs, even though the drugs themselves are not present.

Siegel (1978) proposed the conditional compensatory response model, a classical conditioning model of drug tolerance. In this model, environmental stimuli associated with drug intake become associated with the drug’s effect on the body and elicit a CR that is opposite to the effect of the drug, driven by an automatic drive for body homeostasis. As this CR increases in magnitude with continued drug use, the drug’s effects decrease and tolerance increases. Finally, aversive classical conditioning has been evoked as an additional mechanism by which stimuli associated with the unpleasant periods of drug withdrawal elicit withdrawal-like symptoms. For example, if withdrawal is typically experienced upon waking from sleep, then waking may elicit conditioned withdrawal symptoms that in turn could drive continued drug use to minimize withdrawal effects.