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Article Summary

The Biological Basis of Drug Addiction

The pharmacological activation of brain reward systems is largely responsible for producing a drug's potent addictive properties. Personality, social, and genetic factors may also be important, but the drug's effects on the central nervous system (CNS) remain the primary determinants of drug addiction. Nonpharmacological factors are likely to be important in influencing initial drug use and in determining how rapidly an addiction develops. For some substances, nonpharmacological factors may interact with the drug's pharmacological action to produce compulsive substance use. In these cases, "addictive behavior" may involve use of substances that are generally not considered addictive.

Mesolimbic Dopamine Neurons

Dopamine is one of a number of neurotransmitters found in the central nervous system. Dopamine has received special attention from psychopharmacologists because of its apparent role in the regulation of mood and affect and because of its role in motivation and reward processes. Although there are several dopamine systems in the brain, the mesolimbic dopamine system appears to be the most important for motivational processes. Some addictive drugs produce their potent effects on behavior by enhancing mesolimbic dopamine activity.

Normal Dopamine Activity

Cells in the mesolimbic dopamine system are spontaneously active -- action potentials are constantly generated at a slow rate. This releases small amounts of dopamine into the synaptic cleft. The levels of dopamine produced when the cells are active at this low rate may be responsible for maintaining normal affective tone and mood. Some scientists speculate that some forms of clinical depression may result from unusually low dopamine levels.

Heroin-Enhanced Dopamine Activity

Heroin increases the neuronal firing rate of dopamine cells. The increased number of action potentials produce an increase in dopamine release. The increased dopamine activity increases the effects mediated by postsynaptic dopamine. The heroin user experiences the enhanced dopamine activity as mood elevation and euphoria. When the pharmacological action terminates (i.e., the heroin is eliminated from the brain), the drug user is highly motivated to repeat this experience.

Cocaine-Enhanced Dopamine Activity

Cocaine inhibits the reuptake of dopamine. This increases the availability of dopamine in the synapse and increases dopamine's action on the postsynaptic neurons. The enhanced dopamine activity produces mood elevation and euphoria. Cocaine's effect is usually quite short, prompting the user to repeatedly administer cocaine to re-experience its intense subjective effects.

Combined Heroin- and Cocaine-Enhanced Dopamine Activity

Because heroin and cocaine work on different parts of the mesolimbic dopamine neurons, they can be combined to produce even more intense dopamine activation. (The heroin increases cell firing and dopamine release, while the cocaine keeps the released dopamine in the synaptic cleft longer thereby intensifying and prolonging its effects.) The combination of heroin and cocaine is known by users as a "speed-ball." This combination of drugs is extremely dangerous, and users show very rapid psychological and physiological deterioration.

Although speed-ball use produces extremely intense activation of brain reward systems, it is often short-lived because this drug combination is associated with a very high fatality rate. The combination of cocaine and heroin is perhaps the most dangerous form of illicit substance use; even cocaine and heroin addicts usually avoid this combination of drugs.

Proposed model of brain reward circuitry.

The brain has specialized pathways that mediate reward and motivation. Direct electrical stimulation of the medial forebrain bundle (MFB) produces intensely rewarding effects. Psychomotor stimulants and opiates can also activate this reward system by their pharmacological actions in the nucleus accumbens and ventral tegmental area, respectively. The ventral tegmental action of opiates probably involves an endogenous opioid peptide system (ENK), but the anatomical location of that system has not yet been identified. Natural rewards (e.g., food, sex) and other substances (e.g., caffeine, ethanol, nicotine) may also activate this brain reward system. (From Bozarth, 1987: Ventral Tegmental Reward System. ? 1987 Raven Press)

Neuroadpative Effects

In addition to their acute effects described above, repeated use of psychomotor stimulants like cocaine and opiates like heroin produces changes in the mesolimbic dopamine system. Specifically, repeated use of cocaine or heroin can deplete dopamine from this system. These dopamine depletions may cause normal rewards to lose their motivational significance (i.e., produce motivational toxicity). At the same time, the mesolimbic dopamine system becomes even more sensitive to pharmacological activation by psychomotor stimulants and by opiates (i.e., sensitization develops). These neuroadpative changes are probably critical for producing an addiction. Substances that activate the mesolimbic dopamine system without producing these neuroadaptive effects are probably not truly addictive.

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