The Dopamine System
In the central nervous system, dopaminergic (dopamine-producing) neurons reside only in a few areas, such as the substantia nigra of the midbrain, but establish connections with numerous brain regions. Dopamine (DA) dysfunctions in Parkinson’s disease and schizophrenia, for example, suggest that projections from midbrain to certain brain regions (such as the striatum and frontal cortex) are involved in behavioral reactions controlled by rewards. Extensive studies conducted since the mid-twentieth century revealed that DA is involved in the generation of movement, cognition, attention, mood, reward, reward expectation, addiction, and stress. DA also serves various other functions, including as a hormone helping to stop breast milk flow, as an antipsychotic agent, in the function of the kidneys, and in regulating nausea.
Pleasant behavioral events (natural reinforcers such as eating, drinking, exercising, and sexual activity) stimulate the brain’s reward (limbic) circuitry, causing DA release from dopaminergic neuron terminals. The information is relayed to the frontal lobe of the brain and stored in memory. The stored memory leads to behaviors directed at procuring the reward.
Dopamine in Addiction
Dopamine involvement in multiple stages of addiction is a complex phenomenon and the subject of intense research efforts. The need for DA and its pleasurable effect can be satisfied by substances that mimic the action of this molecule on its receptor.
These substances (addictive drugs) induce transitory, exaggerated increases in DA outside the cells in a deep brain area called nucleus accumbens, a key component of the reward system. This occurs through enhanced release or decreased recycling of the neurotransmitter. The DA surges mimic or exceed the physiological responses that follow natural rewards. A 2015 article published in the journal Nature Reviews Neuroscience suggested that alcohol and stimulants including nicotine, cocaine, and methamphetamine particularly rely on changes in dopamine levels to cause addiction. For other addictive drugs, including heroin, dopamine is thought to be more of a supporting factor in the development of addiction.
Human brain imaging studies demonstrate that the subjective feeling of euphoria occurring during intoxication associated with DA increases in deep brain nuclei. The drug-induced surge of the neurotransmitter is especially rewarding for persons with abnormally low densities of certain DA receptors (such as D2DR). Low receptor availability is associated with an increased risk for abuse of cocaine, heroin, methamphetamine, alcohol, and methylphenidate.
The euphoria triggers a reinforcing pattern that “instructs” the person to repeat the rewarding behavior of abusing drugs. As the abuse continues, long-lasting and significant adaptive decreases in DA brain function occur. These decreased levels reduce the effect of the neurotransmitter on the reward system and force the addicted person to keep abusing drugs in an attempt to normalize DA function.
When larger amounts of the drug are required to achieve the same DA high, desensitization (tolerance) occurs. Chronic drug use ultimately produces cellular and molecular adaptations in higher-processing areas of the brain, leading to disruptions in learning, mood, inhibitory control, and many other functions.
Bibliography
Brookshire, Bethany. "Dopamine Is. . ." Slate. Slate Group, 3 July 2013. Web. 28 Oct. 2015.
Kipper, David, and Steven Whitney. The Addiction Solution. New York: Rodale, 2010. Print.
Koob, George F., and Nora D. Volkow. “Neurocircuitry of Addiction.” Neuropsychopharmacology 35 (2010): 217–38. Print.
Nutt, David J., et al. "The Dopamine Theory of Addiction: 40 Years of High and Lows." Nature Reviews Neuroscience 16 (2015): 305–312. Print.
Renner, John A. Jr., and E. Nalan Ward. “Drug Addiction.” Massachusetts General Hospital Comprehensive Clinical Psychiatry. Eds. Theodore A. Stern et al. St. Louis, MO: Mosby, 2008. Print.
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