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Problem 4. Addiction is a brain disease
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Problem 4. Addiction is a brain diseaseLearning goals
How does the reward system work?
Nestler, E., & Malenka, R. (2004). The addicted brain. Scientific American, 78-85.
Drug abuse produces long-term changes in the reward circuitry of the brain. For many users,
the sight of a drug or its associated paraphernalia can elicit shudders of anticipatory
pleasure. Then, with the fix, comes the real rush: the warmth, the clarity, the vision, the
relief, the sensation of being at the center of the universe. For a brief period, everything
feels right. After repeated exposure to drugs of abuse, users need the drug to feel normal;
without it, they become depressed, and often psychically ill. Then they begin to use the drug
compulsively. At this point, they are addicted, losing control over their use and suffering
powerful cravings even after the thrill is gone and their habit begins to harm their health,
finances and personal relationships.
The euphoria induced by drugs of abuse arises because all these chemicals ultimately boost
the activity of the brain’s reward system: a complex circuit of nerve cells, or neurons, that
evolved to make us feel flush after eating or sex – things we need to do to survive and pass
along our genes. At least initially, goosing this system makes us feel good and encourages us
to repeat whatever activity brought us such pleasure.
Chronic drug use causes changes in the structure and function of the system’s neurons that
last for weeks, months or years after the last fix. These adaptations reduce the pleasurable
effects of a chronically abused substance yet also increase the cravings that trap the addict
in a destructive spiral of escalating use and increased fallout at work and at home.
The brain’s reward circuit consists of the pathway extending from the dopamine-producing
nerve cells (neurons) of the ventral tegmental area (VTA) to dopamine-sensitive cells in the
nucleus accumbens. The changes in this circuit contribute significantly to the tolerance,
dependence and craving that fuel repeated drug use and lead to relapses even after long
periods of abstention.
,Drugs to die for
Stimuli trigger craving and relapse in addicts.
A key component of the reward circuitry is the mesolimbic dopamine system: a set of nerve
cells that originate in the ventral tegmental area (VTA), near the base of the brain, and send
projections to target regions in the front of the brain – most notably to the nucleus
accumbens. Those VTA neurons communicate by dispatching the chemical messenger
(neurotransmitter) dopamine from the terminals of their long projections to receptors on
nucleus accumbens neurons. The dopamine pathway from the VTA to the nucleus
accumbens is critical for addiction.
Rheostat of reward
Several other brain regions serve to color an experience with emotion and direct the
individual’s response to rewarding stimuli, including food, sex and social interaction. The
amygdala, for instance, helps to assess whether an experience is pleasurable or aversive –
and whether it should be repeated or avoided – and helps to forge connections between an
experience and other cues; the hippocampus participates in recording the memories of an
experience, including where and when and with whom it occurred; and the frontal regions
of the cerebral cortex coordinate and process all this information and determine the
ultimate behavior of the individual. The VTA-accumbens pathway acts as a rheostat of
reward: it “tells” the other brain centers how rewarding an activity is. The more rewarding
an activity is deemed, the more likely the organism is to remember it well and repeat it.
, How does the dopamine system change when we use drugs? (short- and long-term effects)
Nutt, D. J., Lingford-Hughes, A., Erritzoe, D., & Stokes, P. R. (2015). The dopamine theory of
addiction: 40 years of highs and lows. Nature Reviews Neuroscience, 305-312
Abstract
For several decades, addiction has come to be viewed as a disorder of the dopamine
neurotransmitter system; however, this view has not led to new treatments. There is robust
evidence that stimulants increase striatal dopamine levels and some evidence that alcohol
may have such an effect, but little evidence, that cannabis and opiates increase dopamine
levels. Moreover, there is good evidence that striatal dopamine receptor availability and
dopamine release are diminished in individuals with stimulant or alcohol dependence but
not in individuals with opiate, nicotine or cannabis dependence. These observations have
implications for understanding reward and treatment responses in various addictions.
Introduction
Addiction is one of the biggest health problems facing the world today. There is a great need
to better understand the brain mechanisms that are involved in addiction so that new,
better-targeted interventions can be developed. Blocking dopamine receptors with
neuroleptic drugs impairs the reinforcing effects of stimulants that results in positive
reinforcement. Dopamine is placed as the central neurotransmitter in stimulant addiction
and suggested that it had roles in reward, motivation and incentive behaviour. Another
study discovered that a range of other drugs of abuse (that is, not only stimulants) increased
dopamine release in the nucleus accumbens, which is located in the ventral striatum.
Dopamine and the drug high
It was proved that the experience of pleasure (the rewarding action) of stimulant drugs in
humans was mediated by striatal dopamine release. Alcohol, tobacco, ketamine and
cannabis increase striatal dopamine release in healthy participants and in non-dependent
drug users, thereby providing support for the dopamine theory of addiction.
The dopamine theory of addiction rapidly became accepted by the field, and drugs that
induce dopamine release were consequently considered to pose a risk of abuse. The
dopamine theory of reward had a profound effect on the development of drugs that target
the brain. Dopamine activity in the ventral striatum is vital in resilience against depression.
Studies of alcohol, cannabis, and ketamine showed that these abused substances do not
inevitably induce dopamine release in humans.
Dopamine became characterized as the ‘pleasure’ neurotransmitter in the human brain –
that is, the one that produces reward. There were doubts about whether this theory applied
to drugs other than stimulants and even whether dopamine release was central to the
rewarding effects of stimulants in humans. It was shown that blocking dopamine receptors
was generally ineffective in blocking the rewarding effects of stimulants in humans or in
treating human addiction (even stimulant addiction). Moreover, several studies found that
opiate administration was not associated with striatal dopamine release in opiate
dependence.
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