Welcome to SALMON the 1998 UCISA award winning website developed by Dr Paul Kenyon (retired) to support students studying evolutionary psychology and behavioral neuroscience in the Department of Psychology, University of Plymouth, Devon, UK
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 systemin the brain. This system is normally activated by natural reinforcers such as food, water, sex etc.
McKim (1997) describes three models of why people become addicted to drugs, or engage in substance abuse to use the modern terminology:
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 addictionas 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
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.
|Effects of heroin||Heroin withdrawal symptoms|
|constipation||diarrhoea & cramps|
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.
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.At one time it was believed that animals could not be made addicted to drugs, but that view is now rejected because technical developments have shown that animals will learn new behaviours that cause injection of drugs into their body.
This diagram shows the apparatus used to study self-administration of drugs in laboratory animals. The rat will learn to press the lever which causes activation of the infusion pump by the program circuitry. The pump delivers drug solution through a catheter implanted into a vein.
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 toleranceto the drug.
The role of classical and operant conditioning are discussed in a separate lecturein this series.
Generally drugs that are self-administered by laboratory animals are also self-administered by humans, and vice versa.
|Drugs that are self-administered by laboratory animals||Drugs that are notself-administered by laboratory animals|
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.
The most popular contemporary view of why humans self-administer potentially lethal drugs is that these chemicals activate the reinforcement systemin the brain. This system is normally activated by natural reinforcers such as food, water, sex etc. Reinforcers are thought to increase the effect of dopamine at receptors in the mesolimbic systemwhich originates in the ventral tegmental areaand terminates in the nucleus accumbens. Crack cocaine is thought to cause a massive and rapid activation of dopamine receptors in this system. Crack users report that the effects are much more intense than those produced by powerful reinforcers such as ejaculation or orgasm.
Reinforcers all share one physiological effect: They increase the release of dopamine (DA) in the nucleus accumbens. This effect can be produced by addictive drugs such as amphetamine, cocaine, opiates, nicotine, alcohol, PCP, and cannabis as well as natural reinforcers such as food, water and sexual contact (White, 1996; Di Chiara, 1995).
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:
Cocaine and amphetamine increase activation of dopamine (DA) receptors and they are thought to act on
This dual-loop system is thought to be critical for reinforcement.
The effects of opioid drugs (heroin and morphine) are less clear cut but Koob (Trends in Pharmacologic Sciences, 13, p177, 1992) suggests they
If the is damaged most reinforcing drugs loose their reinforcing effects.
Images of drug paraphenalia increase metabolic activity (revealed by PET scans) in areas receiving innervation by the Grant et al (cited in Carlson). This was accompanied by the addicts reporting feelings of drug craving. There may be increased D3 DA receptor sensitity in these areas. Stress triggers the release of DA in the nucleus accumbens. Therefore stress may trigger drug-craving.
However this effect does not last.
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
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 compulsionto 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 systemin 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
Figure 1 from Robinson and Berridge (2003)
As you read Robinson and Berridge (2003) consider the following questions: