05-2: Cue Competition & Extinction Effects

Psychology of Learning

Module 05: Classical Conditioning 2

Part 2: Cue Competition & Extinction Effects

Looking Back

In Part 1, we examined taste aversion learning as a challenge to traditional views of classical conditioning. We saw that taste aversions violate several basic principles: they develop after single pairings, tolerate CS-US intervals up to 24 hours, resist extinction, and show selective associations (preparedness). Garcia & Koelling’s (1966) landmark experiment demonstrated that rats readily associate internal cues (flavors) with internal consequences (illness) but external cues (lights and sounds) with external consequences (shock). These findings revealed that organisms aren’t blank slates equally prepared to learn any association—evolution shaped learning mechanisms to capitalize on species-specific sensory strengths and adaptive needs. Now we turn to additional phenomena that challenge simple views of conditioning: cue competition effects showing that stimuli don’t condition independently, drug tolerance as a puzzling case of compensatory conditioning, and extinction effects demonstrating that extinction doesn’t simply erase learning.

Beyond Simple Associations: Cue Competition Effects

Classical conditioning researchers initially adopted the view that all stimuli could be conditioned and become a CS. It should make no difference if the stimulus was visual, auditory, or tactile—pairing it with a US would automatically result in conditioning. Likewise, if several stimuli were simultaneously paired with a US, all would become CSs equally effective in eliciting CRs. However, research revealed these assumptions needed major revision (Kamin, 1969).

Variables Affecting Conditioning Strength

Before exploring cue competition, let’s review variables affecting conditioning strength.

• Salience of CS: More learning occurs with more salient (noticeable, intense) CSs; however, if the CS becomes too salient, it might trigger fear responses that interfere with conditioning.
• Magnitude of US: Larger, more intense USs produce stronger, faster conditioning.
• Contiguity of CS-US: Delay conditioning works best with approximately 0.5-second CS-US intervals (except taste aversions).
• Order of Stimulus Presentation: CS must precede US for effective conditioning.
• Frequency of CS-US Pairing: More acquisition trials generally produce stronger conditioning. These variables seemed to operate independently—until researchers discovered cue competition.

Cue Competition: Stimuli Compete for Predictive Power

Cue competition refers to effects in which the conditionability of a stimulus is influenced by the presence of other stimuli. To-be-conditioned stimuli appear to compete with each other for the ability to become a CS and predict the US. Some stimuli become more strongly conditioned (become better predictors) than others (Kamin, 1969).

If two neutral stimuli are paired with a US—one weak and one strong (salient)—they gain different levels of conditioning. They don’t share conditioning strength equally. Rather, they compete, with the more salient stimulus gaining greater associative strength. This competition reveals that conditioning isn’t automatic—it depends on predictive relationships.

Blocking: Prior Conditioning Prevents New Learning

Blocking occurs when prior conditioning of one stimulus precludes the conditioning of a second stimulus. Even though the second stimulus is perfectly paired with the US, it gains little or no associative strength because the first stimulus already predicts the US (Kamin, 1969).

According to basic classical conditioning theory, simple pairing of a stimulus with a US is necessary and sufficient for establishing that stimulus as a CS. If that’s true, then when the stimulus is paired with the US shouldn’t matter. But blocking demonstrates this is wrong. Conditioning is not automatic—conditioning occurs only if the CS can help predict the US better than existing cues.

Kamin’s (1969) classic blocking experiment used a two-phase design. In Phase 1, the experimental group receives tone (CS1) paired with shock (US) until strong fear conditioning develops, while the control group receives no training. In Phase 2, both groups receive compound stimulus (tone + light) paired with shock; the tone is CS1 (already conditioned for experimental group), and light is CS2 (new for both groups). At test, when light (CS2) is presented alone, the control group shows strong fear CR to light—they learned the light predicts shock. The experimental group shows weak or no CR to light—prior tone conditioning blocked light conditioning! The tone already predicted shock perfectly, so the light provided no new information. Learning occurs only when events are surprising or informative.

Blocking in Cancer Treatment

Bernstein & Webster (1980) applied blocking to help cancer patients. Chemotherapy (US) produces nausea (UR), often causing patients to develop taste aversions to foods eaten before treatment. These aversions can lead to malnutrition and reduced quality of life. How can we prevent these aversions?

Patients ate breakfast (CS1), then were given Mapletoff-flavored ice cream (CS2) before chemotherapy (US). Later, when presented with Mapletoff ice cream (CS2), patients consumed less—they developed aversions to it (CR). But critically, this taste aversion blocked other taste aversions that often occur with chemotherapy (aversions to breakfast foods, CS1). The scapegoat ice cream took the “blame” for nausea, protecting nutritionally important foods from becoming aversive. This clever application of blocking principles improved patient outcomes (Bernstein & Webster, 1980).

Overshadowing: Salient Cues Dominate Compound CSs

Overshadowing occurs when one stimulus in a compound CS is easier to condition and, therefore, gains more associative strength with the US. The more salient stimulus overshadows the less salient stimulus, even though both are presented simultaneously (Pavlov, 1927).

When a compound CS is used, the total amount of conditioning remains constant, but each element in the compound CS gains some strength. They don’t share equally—more salient stimuli gain more strength. An experimenter might present a compound stimulus consisting of a loud tone (CS1) and weak light (CS2) followed by food (US). Testing reveals stronger conditioning to the loud tone—it overshadowed the weak light (Mackintosh, 1976).

Overshadowing differs from blocking. In blocking, stimuli are presented sequentially (CS1 first, then CS1+CS2). In overshadowing, stimuli are presented simultaneously from the start as a compound CS. Both demonstrate cue competition, but through different mechanisms.

Potentiation: When Compound CSs Enhance Learning

Cue facilitation occurs when pairing a compound CS with a US results in enhanced conditioning to one of these cues. Potentiation refers specifically to the enhancement of a CS’s ability to elicit a CR by pairing it with another stimulus during conditioning (Rusiniak, Hankins, Garcia, & Brett, 1979).

Potentiation is the opposite of overshadowing. Instead of stimuli competing for associative strength, the presence of multiple cues enhances learning. This typically occurs in taste aversion learning with odor-taste compounds.

Rusiniak et al. (1979) demonstrated potentiation: Rats received either a compound CS (weak odor + strong novel flavor) or single CS (weak odor alone), followed by illness induction. Rats receiving the compound stimulus exhibited stronger odor aversion than rats receiving only odor-illness pairing. The presence of taste potentiated (enhanced) conditioning to odor! When conditioned alone, the weak odor produced weak aversions. But when paired with a strong taste, the odor gained substantial associative strength.

Why does potentiation occur? In taste aversion learning, odors and tastes naturally co-occur—foods have both properties. Organisms benefit from learning about both simultaneously. The taste helps “highlight” the odor, making it more noticeable and conditionable. This represents another biological constraint on learning—certain stimulus combinations facilitate rather than compete.

Drug Tolerance as Classical Conditioning

Mimicking Versus Compensatory CRs

We’ve typically assumed CRs resemble URs—salivation to a tone mirrors salivation to food. But not all CRs mimic URs. A mimicking CR is a CR similar to the UR, like salivation in Pavlov’s experiments; the CR resembles what the US produces (Pavlov, 1927). A compensatory CR is a CR opposite to the UR and seems to compensate for the UR’s effects; the CR opposes rather than mimics the UR (Siegel, 1975).

Why would CRs sometimes oppose URs? Remember, CRs prepare organisms for upcoming events. The key question becomes: What are we preparing for? Sometimes preparation means mimicking the upcoming response. Other times, preparation means counteracting it. Drug tolerance provides a compelling example.

Tolerance & Contextual Conditioning

Tolerance is the decrease in a drug’s effectiveness with repeated use. Users need increasingly larger doses to achieve the same effect. Traditional theories attributed tolerance to increased metabolic capacity—bodies becoming more efficient at breaking down drugs. But classical conditioning provides an alternative explanation (Siegel, 1975).

According to the conditioning account, contextual stimuli associated with drug use act as CSs: the environment where drugs are taken, drug paraphernalia (needles, pipes), early bodily sensations from drug administration. These CSs become associated with drug effects (US). Through conditioning, these cues elicit compensatory CRs—responses opposite to the drug’s effects—that prepare the body for the drug’s impact.

Siegel’s Morphine Tolerance Research

Siegel (1975) tested whether context acts as a CS creating compensatory CRs. His elegant experiment used morphine’s analgesic (pain-reducing) effects. Pain sensitivity was measured by the time before rats licked their paws exposed to uncomfortably hot temperature (54°C); longer latencies indicate greater pain tolerance (analgesia).

The Control Group was tested repeatedly without morphine and showed no change across trials—stable pain sensitivity. The Morphine Group was given morphine before pain testing; the first trial showed decreased pain sensitivity (morphine’s analgesic effect), but this effect disappeared over trials—rats exhibited tolerance to the drug. With repeated exposures, morphine became less effective. The Context Group received morphine in the same environment for three trials (like morphine group), developing tolerance. But on the fourth trial, they were moved to a different environment. Result: Tolerance disappeared! They showed the same strong morphine effect as on the first trial. The original context was creating tolerance by becoming a CS eliciting compensatory CRs. In the new context, without conditioned compensatory responses, morphine’s full effects returned (Siegel, 1975).

This experiment demonstrates that tolerance isn’t just metabolic adaptation—it’s learned, context-dependent compensation.

Contemporary Neuroscience of Pavlovian Drug Tolerance

Recent neuroscience research has identified specific neural mechanisms underlying Pavlovian-conditioned opioid tolerance. Siciliano (2023) highlighted that Siegel’s behavioral findings from the 1970s—showing that analgesic tolerance depends on morphine-associated cues and can be extinguished when those cues are absent—have been validated and extended through modern neural circuit analysis. Contemporary studies reveal that conditioned tolerance involves coordinated activity in specific brain pathways that learn to anticipate drug effects. When opioid-conditioned cues are presented, these circuits initiate compensatory physiological responses that counteract the anticipated drug effect before the drug even takes effect. This research demonstrates that what appears as simple pharmacological tolerance is actually a sophisticated form of associative learning, with distinct neural substrates mediating the acquisition, expression, and extinction of conditioned drug responses. These findings have important implications for understanding individual differences in overdose vulnerability and for developing treatments that target the associative components of addiction.

Human Examples: Coffee & Heroin

For humans, caffeine (US) leads to salivation (UR). After tolerance to coffee develops, coffee consumption produces very little salivation. Presumably, the sight and smell of coffee (CS) elicit compensatory CR (inhibition of salivation). When actual coffee is consumed, the net salivation (CR- + UR+ = very little) is much less than initially.

When experienced coffee drinkers consumed decaf coffee, they exhibited decreased salivation—the sight and smell still acted as CS, producing compensatory CR (decreased salivation), but no actual caffeine arrived to produce UR (increased salivation). The compensatory response appeared unopposed. The same drinkers experienced substantially increased salivation when given caffeinated apple juice—no CS present to elicit compensatory CR, so the caffeine UR appeared at full strength (Siegel, 2005).

Most tragically, a large portion of heroin overdoses don’t occur because the dose was particularly high, but because it was taken in a different environment where contextual cues couldn’t act as CSs eliciting compensatory CRs. Without these conditioned protective responses, even a typical dose can prove fatal. Understanding drug tolerance as classical conditioning has life-or-death implications (Siegel, Hinson, Krank, & McCully, 1982).

Extinction: More Than Simple Forgetting

Extinction occurs when the CS is presented without the US, leading to gradual reduction in CR strength. Simple theory suggests extinction gradually weakens the CS-US association until it’s eliminated—essentially, extinction is forgetting. But if associations are forgotten, how do we explain spontaneous recovery? Multiple lines of evidence demonstrate extinction isn’t forgetting—it’s new learning that coexists with original learning.

Facilitated Reacquisition

Facilitated reacquisition occurs when an extinguished CR is reconditioned more rapidly than original conditioning. If extinction completely eliminated the CS-US associative bond, reconditioning should take as long as original conditioning. The fact that CRs reappear more rapidly shows that, even when CRs aren’t shown and experimenters conclude extinction is complete, some association between CS and US still exists. Extinction is not the same as forgetting (Rescorla, 2001).

Imagine conditioning a tone-shock association, extinguishing it, then reconditioning. Reacquisition occurs much faster than original acquisition—often within just a few trials. The original learning wasn’t erased; it was suppressed by extinction learning. When the US returns, the suppressed association quickly reemerges.

Renewal of the CR

Renewal refers to the return of an extinguished CR when testing occurs in the original conditioning context after extinction in a different context. The basic procedure involves three phases: (1) condition a fear response in a specific, distinctive environment, (2) extinguish the CR in a second, very different environment, (3) test for the CR in the first environment. Result: CR returns in the original environment (Bouton & Bolles, 1979).

Renewal differs from spontaneous recovery. In spontaneous recovery, passage of time is the key variable—wait long enough after extinction and CRs reappear. In renewal, environments where conditioning, extinction, and testing occur are paramount. Return to the conditioning context and extinguished CRs return, even without time passage (Bouton, 1993).

Occasion setting occurs when a particular stimulus or environment (the occasion setter) helps retrieve a specific memory. Contexts become occasion setters during conditioning—they signal which learning (original conditioning or extinction) is currently relevant. The conditioning context retrieves the CS-US association; the extinction context retrieves the CS-no US association (Bouton, 1993).

Renewal has important clinical implications. Phobia treatments using exposure therapy (extinction) often work well in the clinic but relapse occurs when patients return home. The home environment, where the phobia originally developed, triggers renewal. Successful treatments must address context-dependency—conducting exposure in multiple contexts helps prevent renewal.

Looking Forward

We’ve explored cue competition (blocking, overshadowing, potentiation), demonstrating that stimuli don’t condition independently—they compete for or facilitate associative strength based on their predictive value. We examined drug tolerance as compensatory classical conditioning, revealing that CRs can oppose URs to prepare for drug effects. We explored extinction effects (facilitated reacquisition, renewal) showing extinction creates new, context-dependent learning rather than erasing original associations. In Part 3, we’ll examine theoretical accounts attempting to explain these complex findings: Pavlov’s stimulus substitution theory, the Rescorla-Wagner model emphasizing prediction errors and surprise, and the comparator hypothesis focusing on relative predictiveness. Understanding these theories provides deeper insight into the computational problems organisms solve through associative learning.