The Relationship between the CR and the UR
In Pavlov’s original studies, dogs salivated both when they heard the CS and when they experienced the US. We might conclude from this that the conditioned response (CR) and unconditioned response (UR) are essentially the same behavior—and simply triggered by different inputs. In truth, though, the CR and UR are rarely identical and are sometimes quite different from each other.
Consider, for example, a rat that has been conditioned to associate a flashing light with electric shock. When the shock is actually presented, the animal jumps and squeals, and its heart beats faster; this is the UR, triggered by the shock itself (the US). When the animal sees the flashing light, though, its response (the CR) is different. The animal freezes and tenses its muscles, and its heartbeat slows. This is not an escape-from-shock reaction; instead, it’s a display of fearful anticipation.
From a biological perspective, this result makes sense. A flashing light causes no phys-ical damage, and so there’s no need to spend energy escaping from the light. Likewise, an animal can’t eat a tone that has been paired with food, so there’s no point in opening its mouth and chewing in response to the tone. In these and many other cases, it’s sensible for the animal to react somewhat differently to the CS than it does to the US.
So, what is the relationship between the conditioned response (CR) and the uncondi-tioned response (UR)? We’ve already seen that animals interpret the CS as a signal indicat-ing that the US is about to arrive. Plausibly, then, we can think of the CS as telling the animal to “Get ready!”—and, from this perspective, the CR is just the set of adjustments the animal makes in preparation for the US. If the sound of a bell has been reliably followed by food, then the sound now signals that the animal should moisten its mouth so it will be ready to eat when the food arrives. If the sight of a light has been followed by a shock, then the light is a signal that the animal should stop moving around and stay at “full alert” so it will be ready to jump as soon as the shock begins (Domjan, 2005; P. Holland, 1984; Hollis, 1984).
Does this preparation help the animal? It surely does. Evidence suggests, for example, that sexual activity is more likely to lead to offspring if a CS announced the imminent arrival of the US (the sight of a sexually receptive partner). Presumably, this is because the CS allowed the animal to prepare itself for mating (Domjan, 2005). Likewise, digestion is more efficient if a CS announced the imminent arrival of the US (food in the mouth); again, the CS allowed the animal to prepare to ingest and digest the food (Domjan, 2005; Woods & Ramsay, 2000).
Preparation for a US can take many forms. As a remarkable illustration, consider the sit-uation of a heroin addict. The heroin itself is a potent stimulus with many biological effects: It decreases pain sensitivity and lifts the user’s mood. It also causes other changes throughout the body, including drying out the mouth and various mucous membranes.
The first few times someone uses heroin, all of these effects are strong. If drug use continues, though, these effects diminish. This phenomenon, which we described, is called drug tolerance—a decrease in the response to a drug, usually result-ing from continued use. If the person wants to keep getting the same impact from the drug, they’ll need a larger and larger dose to offset the effect of the tolerance.
Continued use of heroin also leads to drug dependence and drug cravings—an inabil-ity to function without the drug and an overwhelming desire for yet another dose, yet another injection. The cravings are accompanied by their own set of effects—including an increased sensitivity to pain, a depression in the person’s mood, and an overproduc-tion of fluid in the person’s mouth and mucous membranes.
What’s going on here? What produces drug tolerance and drug craving? Why does the craving take the form that it does? Answers to these questions turn out to include a key role for classical conditioning. To understand how this works, however, we need to begin with a point we’ll discuss more fully later where we consider the importance of homeostasis. This term refers to the remarkably stable environment that exists inside ofour bodies—a body temperature that’s kept at an almost constant level, a nearly constant pH in the bloodstream, a consistent level of glucose and oxygen in the blood, and so on.
A drug such as heroin changes the body’s status in many ways. In other words, heroin disrupts homeostasis; and so, when this drug is present in the body, a range of mechanisms come into play, all seeking to restore homeostatic stability. These mecha-nisms involve many cellular and biochemical changes throughout the body—all designed to repair the “disruption” caused by the drug.
But, of course, preventing a problem is always preferable to solving the problem after it arises; avoiding disruption is better than repairing the disruption once it’s in place. Rather than waiting until heroin disrupts the body’s state and then responding to this disruption, it would be better if the body had a way of dealing with the heroin disrup-tion as it happens, so that homeostasis is never lost in the first place. This is where clas-sical conditioning enters the scene: Thanks to conditioning, the body begins a series of adjustments to offset the heroin’s effects even before the drug arrives.
Let’s put this in concrete terms. For a heroin user, the US is the drug itself; the UR is the body’s natural response to the drug (Figure 7.15). The CS is complex and includes all the stimuli that signal the drug is about to arrive—the sight of the needle, thoughts about the drug, possibly the sights and smells of the physical environment in which the drug is injected, and so on. But what is the CR? Here as always, the CR will be a response that prepares the organism for the US, and so we need to ask: What is the right preparation for heroin? If the goal is homeostasis, then the CR should include a depression of mood in order to cancel out heroin’s positive effects on mood; it should also include an increase in pain sensitivity to cancel out heroin’s analgesic effects; it should include an increase in moisture in the mucous membranes to offset heroin’s tendency to dry out these membranes. In point after point, the CR should simply be the opposite of the UR, so that the two will cancel each other out, leaving no overall effect—and thus preserving homeostasis. A CR like this is referred to as a compensatory response—one that “compensates” for the effects of the upcoming US.
Of course, when someone is exposed to heroin for the first time, there hasn’t yet been an opportunity for learning. Therefore, the US (the heroin) will produce the UR
(the biological reaction to the drug); but there will be no CR (because no learning has taken place yet). As a result, the person will experience the drug’s full effects, and no compensatory response will be in place (Figure 7.15, top panel). After repeated expo-sures to the drug, though, learning will have taken place. At this point the US still pro-duces the UR; but now, in addition, the CS elicits the compensatory CR. This learned response, we’ve proposed, functions to “cancel out” the heroin effects and preserve homeostasis. As a result, the UR will be less evident—resulting in the diminished drug response that we call drug tolerance (Figure 7.15, middle panel).
What happens if an addict sees an empty hypodermic needle, or visits the place where he ordinarily buys or injects the drug, but no heroin is available (Figure 7.15, bottom panel)? In these cases the drug-associated signals all indicate that the drug will arrive soon, but then it never arrives—so there’s a CS (the signals), but no US (no heroin). With the CS present, the CR will be produced; but with no US, there will be no UR. As a result, the person will experience the CR on its own—and the CR, we’ve proposed, is the opposite of the UR. Hence the person experiences the depression, the pain sensitivity, and so on—exactly the pattern referred to as drug craving.
Many experiments have confirmed these claims about heroin tolerance and craving. Among other points, the data indicate that tolerance shows not only the pattern of gen-eralization and discrimination that we would expect with classical conditioning but also the familiar patterns of extinction and spontaneous recovery. In other words, tol-erance shows the standard profile of classical conditioning, and this is strong support for the account we’ve just sketched. Moreover, related studies show a similar role for conditioning in tolerance observed with other drugs, including insulin, nicotine, caf-feine, and amphetamines (Domjan, 2005; S. Siegel, 1977, 1983; S. Siegel & Allan, 1998; S. Siegel, Kim, & Sokolowska, 2003; Sokolowska, Siegel, & Kim, 2002). Overall, these points provide a powerful argument that the CR is indeed best understood as a prepa-ration for the US; but it’s important to note that this notion of preparation must beunderstood broadly.
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