Drug Addiction Overview Theories of Drug Addiction Physical Dependency Model Positive Reinforcement Model Drugs and Brain Reinforcement Systems What is the role of dopamine in reward? Seminar discussion themes References and further reading Online resources Further reading Visit the SALMON Bookshop for recommended books on this topic

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Overview : This lecture is concerned with why people take drugs. Three models are considered:

• the disease model
• the physical dependency model
• the positive reinforcement model

The main focus of the lecture is on the positive reinforcement model. The most popular contemporary view of why humans self-administer potentially lethal drugs is that these chemicals activate the reinforcement system in the brain. This system is normally activated by natural reinforcers such as food, water, sex etc.

Theories of Drug Addiction

McKim (1997) describes three models of why people become addicted to drugs, or engage in substance abuse to use the modern terminology:

• the disease model
• the physical dependency model
• the positive reinforcement model

At one time people with problems associated with alcohol or other drugs were regarded as sinners or criminals, and any help they might receive came via the courts or the church. Towards the end of the 19th century the medical profession began to use the word addiction as both an explanation for, and diagnosis of, excessive drug use. This idea was formalized in the 1950s when the World Health Organization (WHO) and American Medical Association (AMA) classified alcoholism as a disease. One consequence of this change in attitude is the notion that the addict is not in control of their behaviour, that they require treatment rather than punishment.

One problem with the disease model is that it not clear how one catches this disease. The presence of withdrawal symptoms led to the idea that the avoidance of withdrawal symptoms was the reason people continued to self-administer drugs. This is the essence of the physical dependency model

Physical Dependency Model

After repeated exposure to certain drugs, withdrawal symptoms appear if the drug is discontinued.

Withdrawal symptoms are compensatory reactions that oppose the primary effects of the drug. Therefore they are the opposite of the effects of the drug.

Withdrawal effects are unpleasant and reduction in these effects would therefore constitute negative reinforcement . [Negative reinforcement is the reinforcement of behaviour that terminates an aversive stimulus] Negative reinforcement could explain why addicts continue to take the drug. However some addicts will endure withdrawal symptoms ( go 'cold-turkey') in order to reduce their tolerance so that they can recommence drug intake at a lower dose which costs less to purchase.

Concentrating on the role of physical withdrawal effects at the expense of other psychological factors led to the failure to recognize the addictive properties of cocaine. Cocaine does not produce physical dependency (tolerance and withdrawal symptoms) but it is more addictive than heroin. This diagram (redrawn from Julien, 1995), shows the changing pattern in the major drug used by patients admitted to drug treatment programs in New York City during the 1980s. It is also important to emphasize that reduction in withdrawal symptoms does not explain why people take drugs in the first place. Negative reinforcement may account for initial drug taking in some situations. For example, someone who is suffering from unpleasant emotions may experience a reduction in these feelings (i.e. negative reinforcement) following drug administration. However the most likely reason for drug taking involves positive reinforcement.

Positive Reinforcement Model

The reinforcing properties of a drug are thought to be reason why most people become addicted to drugs.

Addictive drugs are positive reinforcers (Carlson, 2001). As you know positive reinforcement can lead to learning a new response, and the maintenance of existing behaviours. It follows that the behaviours associated with taking an addictive drug (i.e. injecting or smoking it) will increase in probability. One way of testing this claim is to examine the reinforcing properties of drugs in animals. We already know that conventional reinforcers support bar-pressing in animals, therefore if a drug maintains a response such as bar-pressing in an animal, it is a reinforcing stimulus.

This figure shows the daily amount of morphine self-administered by a monkey over 25 weeks. The daily intake is redrawn from data reported by Deneau et al, (1969). I have added the trend line to show the progressive increase in intake which may reflect growing tolerance to the drug.

The role of classical and operant conditioning are discussed in a separate lecture in this series.

Generally drugs that are self-administered by laboratory animals are also self-administered by humans, and vice versa .

Note that procaine (structurally similar to cocaine, normally used as a dental anaesthetic) is self-administered by laboratory animals, but it is not abused by humans. Mescaline is taken by humans, but animals will not self-administer it.

Drugs and Brain Reinforcement Systems

As an example of this effect of reinforcers, Phillips found that that DA is released from the nucleus accumbens when a rat presses a lever that delivers reinforcing brain stimulation to its ventral tegmental area (VTA) (Phillips et al, 1992).

In this experiment:

• an electrode (thin wire) was implanted with its tip in the VTA
• electrical stimulation is delivered through this electrode when the rat presses a lever
• the mesocorticolimbic system projects forwards from the VTA to the nucleus accumbens
• DA is collected through a cannula (thin hollow tube) with its tip positioned in the nucleus accumbens
• notice how the release of DA coincides with the rat delivering reinforcing electrical stimulation to its VTA.

What is the role of dopamine in reward?

According to most textbooks when the dopamine pathway running from the  ventral tegmental area to the nucleus accumbens in the forebrain is activated, the  release of dopamine into the forebrain nucleus accumbens is believed to cause feelings of pleasure. However this conventional view has been challenged by Dr. Mark Wightman  and his colleagues (Garris et al, 1999) at the University of North Carolina (see Center Line (2000)). They confirmed   previous findings that:

• Artificially stimulating the ventral tegmental area at a regular or irregular rate released dopamine in the forebrain.
• Rats can be trained to electrically stimulate the ventral tegmental area.
• Rats were unable to learn to self-stimulate if the stimulation produced no dopamine release
• As predicted this self-stimulation is accompanied by the release of dopamine in the forebrain

However this effect does not last.

• With continued training  virtually no dopamine was released in response to self-stimulation of the ventral tegmental area, even though ventral tegmental stimulation remained rewarding—the animal continued performance of the bar pressing response.

Therefore the release of dopamine may not be critical for reinforcement once the task is learned. Wightman has suggested that  dopamine may   be a neural substrate for novelty or reward expectation rather than reward itself.

Seminar discussion themes

Read Robinson and Berridge (2003). Addiction. Annual Reviews of Psychology, Vol 54, available online

The World Health Organization (WHO) stress that drug dependence always includes "a compulsion to take the drug on a continuous or periodic basis". As we have seen the most popular contemporary view of why humans self-administer potentially lethal drugs is that these chemicals activate the reinforcement system in the brain. This mechanism may explain why some people initially take potentially addictive drugs, but there are several aspects of addiction that may not be explained by the theory.

Robinson and Berridge (2003) point out that

• although a significant number of people take potentially addictive drugs at some time during their lives, relatively few become addicts. We know relatively little about the psychological factors that are involved in the 'transition to addiction'.
• sometimes addicts take drugs to escape from drug-withdrawl states, but withdrawl states are not very powerful in motivating drug-seeking behaviours. As one addict put it:
  "No doc, craving is when you want it—want it so bad you can almost taste it ...but you ain’t sick ...sick is, well sick" (Childress et al.1988).

Figure 1 from Robinson and Berridge (2003)

As you read Robinson and Berridge (2003) consider the following questions:

• Explain the opponent process theory of drug addiction.
• What is more effective - a priming drug injection, or precipitated withdrawl - in producing relapse into drug taking behaviour? What are the implications of your answer for  the opponent process theory?
• Is relapse after detoxification programs consistent with opponent process theory?
• Does drug addiction involve 'explicit learning'?
• What aspects of a drug addict's behaviour could be explained in terms of 'implicit learning'?
• Explain the incentive-sensitization theory of addiction.
• What is the difference between drug 'liking' and drug 'wanting' ?
• What is drug 'sensitization'?
• Can sensitization explain individual differences in drug addiction?
• Can the concept of drug 'wanting' be measured behaviourally?
• Can sensitization explain relapse in detoxified drug addicts?

References

• Carlson (2001). Physiology of Behavior, Allyn and Bacon, Boston.
• Center Line (2000). New insights on the neural basis of brain reward and alcohol drinking. In Center Line Volume 11, Number 2, 2000 published by UNC Bowles Center for Alcohol Studies School of Medicine, University of North Carolina at Chapel Hill. Available online
• Deneau et al. (1969). Psychopharmacologia (Berlin) 16, 30-48.
• Di Chiara (1995). Drug and Alcohol Dependency, 38, 95-137.
• Garris, P.A., Kilpatrick, M., Bunin, M.A., Michael, D., Walker, Q.D., and Wightman, R.M. Nature 398, pp. 67-69, 1999.
• Julien (1995). A Primer of Drug Action, 7th Ed, Freeman, New York.
• McKim (1997). Drugs and Behavior , 6th Ed, Prentice Hall, New Jersey.
• Phillips et al, (1992). Annals of the New York Academy of Sciences, 654, 199-206.
• Robinson and Berridge (2003). Addiction. Annual Reviews of Psychology, Vol 54, available online
• White (1996). Annual Review of Neurosciences, 19, 405-436.

Online resources

• Addiction Science Network (ASNet) is a virtual network for the scientific study of addiction and for the application of information derived from scientific analysis to the problems of addiction.
• Addiction Science Network (2000). The Biological Basis of Addiction
• Bozarth (1994). Pleasure systems in the brain. In D.M. Warburton (ed.), Pleasure: The politics and the reality (pp. 5-14 + refs). New York: John Wiley & Sons
• Koob, Sanna , Bloom (1998) . Neuroscience of Addiction. Neuron, Vol 21, 467-476, September, 1998. PDF copy
• Nestler (2002). The Genetic Basis of Addiction. Psychiatric Times, February 2002  Vol. XIX  Issue 2
• Pistoi (2001). Study Reveals Why People Might Crave Cocaine. Scientific American May 11, 2001
• Powledge (2002). Beating Abuse: Glutamate may hold a key to drug addiction . Scientific American, January 15, 2002.
• Robbins and Everitt (1999). Drug addiction: bad habits add up. Nature 398:567-570, 1999. PDF copy
• Robinson and Berridge (2003). Addiction. Annual Reviews of Psychology, Vol 54, available online
• Sullivan and Hagen (2002) Psychotropic substance seeking: evolutionary pathology or adaptation? Addiction 97:389-400.
• Wise (1996). Neurobiology of addiction, Current Opinion in Neurobiology, 6:243-251, 1996. PDF copy