Throughout this chapter we have concluded repeatedly that animals engage in a wide range of voluntary behaviors because those behaviors are rewarding. That is, they increase the activity in neural circuits that function to maintain an animal’s contact with certain environmental stimuli, either in the present or in the future. Presumably, the animal perceives the activity of these circuits as pleasant. This would explain why reward can help maintain not only adaptive behaviors such as feeding and sexual activity but also potentially nonadaptive behaviors such as drug addiction. After all, evolution would not have prepared the brain specifically for the eventual development of psychoactive drugs.

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The first clue to the presence of a reward system in the brain came with an accidental discovery by James Olds and Peter Milner in 1954. They found that rats would perform behaviors such as pressing a bar to administer a brief burst of electrical stimulation to specific sites in their brain. This phenomenon is called intracranial self-stimulation or brain stimulation reward.

Typically, rats will press a lever hundreds or even thousands of times per hour to obtain this brain stimulation, stopping only when they are exhausted. Why would animals engage in such behavior when it has absolutely no survival value to them or to their species? The simplest explanation is that the brain stimulation is activating the system underlying reward (Wise, 1996).

After more than a half-century of research on brain stimulation reward, investigators now know that dozens of brain sites maintain self-stimulation. Some especially effective regions are the lateral hypothalamus and medial forebrain bundle (see Figures 12-12 and 12-13). Stimulation along the MFB tract activates fibers that form the ascending pathways from dopamine-producing cells of the midbrain tegmentum, shown in Figure 12-28. This mesolimbic dopamine pathway sends terminals to sites that include especially the nucleus accumbens in the basal ganglia and the prefrontal cortex.

Neuroscientists have several reasons to believe that the mesolimbic dopamine system is central to circuits mediating reward:

Even opioids appear to affect at least some of an animal’s actions through the dopamine system. Animals quickly learn to press a bar to obtain an opioid injection directly into the midbrain tegmentum or the nucleus accumbens. The same animals do not work to obtain the opioid if the dopaminergic neurons of the mesolimbic system are inactivated. Apparently, then, animals engage in behaviors that increase dopamine release.

Nor is dopamine the only rewarding compound in the brain. For example, opioid transmitters such as encephalin and dynorphin are also rewarding, as are benzodiazepines.

Robinson and Berridge (2008) propose that reward contains separable psychological components corresponding roughly to wanting, which is often called incentive, and liking, which is equivalent to an evaluation of pleasure. This idea can be applied to discovering why we increase contact with a stimulus such as chocolate.

Two independent factors are at work: our desire to eat the chocolate (wanting) and the pleasurable effect of eating the chocolate (liking). This distinction is important. If we maintain contact with a certain stimulus because dopamine is released, the question becomes whether the dopamine plays a role in the wanting or the liking aspect of the behavior. Robinson and Berridge propose that wanting and liking processes are mediated by separable neural systems and that dopamine is the transmitter for the wanting. Liking, they hypothesize, entails opioid and benzodiazepine–GABA systems.

According to Robinson and Berridge, wanting and liking are normally two aspects of the same process, so rewards are usually wanted and liked to the same degree. However, it is possible, under certain circumstances, for wanting and liking to change independently.

Consider rats with lesions of the ascending dopaminergic pathway to the forebrain. These rats do not eat. Is it simply that they do not desire to eat (a loss of wanting), or has food become aversive to them (a loss of liking)? To find out which factor is at work, the animals’ facial expressions and body movements in response to food can be observed to see how liking is affected. After all, when animals are given various foods to taste, they produce different facial and body reactions, depending on whether they perceive the food as pleasant or aversive.

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Among humans, typically when a person tastes something sweet, he or she responds by licking the fingers or the lips, as shown at the left of Figure 12-29. If the taste is unpleasantly salty, say, as shown in the right panel, the reaction is often spitting, grimacing, or wiping the mouth with the back of the hand. Rats, too, show distinctive positive and negative responses to pleasant and unpleasant tastes.

By watching the responses when food is squirted into the mouth of a rat that otherwise refuses to eat, we can tell to what extent a loss of liking is a factor in the animal’s food rejection. Interestingly, rats that do not eat after receiving lesions to the dopamine pathway act as though they still like food.

Now consider a rat with a self-stimulation electrode in the lateral hypothalamus. This rat will often eat heartily while the stimulation is on. The obvious inference is that the food must taste good—presumably even better than usual. But what happens if we squirt food into the rat’s mouth and observe its behavior when the stimulation is on versus when it is off?

If the brain stimulation primes eating by evoking pleasurable sensations, we would expect the animal to be more positive in its facial and body reactions to foods when the stimulation is turned on. In fact, the opposite occurs. During stimulation, rats react more aversively to tastes such as sugar and salt than when stimulation is off. Apparently, the stimulation increases wanting but not liking.

Such experiments show that what appears to be a single event—reward—is actually composed of at least two independent processes. Just as our visual system independently processes what and how information in separate streams, our reward system appears to process wanting and liking independently. Reward is not a single phenomenon any more than perception or memory is.

Like the networks underlying perception and memory, the prefrontal and limbic networks underlying reward are diffuse. Amy Janes and her colleagues (2012) used resting-state fMRI to identify a prefrontal–anterior cingulate network believed to support reward, illustrating the breadth of the reward system. They then compared these networks in nicotine addicts and nonaddicts finding greater connectivity in the prefrontal–striatal connections in nicotine addicts. In a follow-up study the investigators also showed that craving in nicotine addicts is related to enhanced connectivity in this prefrontal network (Figure 12-30). (Janes et al., 2014).

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The general conclusions from these studies and from related studies of gamblers are that neural reward pathways are diffuse and that the pathways’ size and activity are related to the reward’s intensity. The hope is that rs-fMRI can be used as a biomarker for both severity of addiction and efficacy of treatment. But the extent of addiction-related changes suggests that eliminating nicotine addiction is not easy—a conclusion many nicotine addicts would agree with.

Reward

Before you continue, check your understanding.

Question 1

Question 2

Question 3

Question 4

Answers appear in the Self Test section of the book.