Addiction includes compulsive seeking of drugs of abuse. These drugs produce positive emotional states following intake, but may lead to negative feelings in their absence. Multiple approaches will be necessary to understand addiction. However, we can assume that part of our understanding will come from exploration of molecules and brain circuitry that predispose to addictive behaviour, and change after drug experimentation. We examine these ideas, focusing on the ‘reward pathway’ in the brain. Addiction studies, in addition to combating a major scourge of society, offer an opportunity to understand mechanisms of neural plasticity important to the brain's ability to learn.

Key Concepts

  • Addiction refers to compulsive use of a class of drugs known as ‘drugs of abuse’.

  • The ‘reward pathway’ in the brain is a major target of drugs of abuse.

  • The initial positive feelings generated by these drugs can diminish with use, and may reduce the reward derived from previously rewarding nondrug experiences.

  • Addiction can be understood in terms of molecules and brain circuits that may differ in individuals and predispose to addictive behaviour, and may change as a result of drug experimentation, leading to compulsive drug use.

  • Many of the important issues of neuroscience can be examined within the context of addiction. These include the brain mechanisms of reward, genetic predisposition to behaviours, and neuronal plasticity.

Keywords: tolerance; alcohol; opiates; channels; addiction

Figure 1.

Drugs of abuse affect the gating of individual neuron channels. These figures are schematics of the opening and closing of two classes of ion channel that control release of neurohormones from nerve terminals in the posterior pituitary of the brain. The technique used to obtain this type of data is single‐channel patch clamp recording. (a) It can be seen that, in the presence of alcohol, each opening of the voltage‐gated calcium channel has a shorter duration than in the absence of the drug. (b) The converse is seen when another channel, the calcium‐activated potassium channel, is examined. In this case, the closed periods in channel activity are shortened, leading to a greater overall open time. The reduction of activity of the voltage‐gated calcium channel, coupled with the increased activity of the calcium‐activated potassium channel, leads to decreased hormone release.

Figure 2.

Repeated drug exposure changes the brain's response to the drug. The plots indicate that for a given level of drug effect, a greater amount of drug is necessary after repeated exposure, typical of the phenomenon of tolerance. Although no units are shown, the shapes of the curves are characteristic of plots in which the drug concentration (the abscissa) is plotted on a logarithmic scale.

Figure 3.

The reward threshold is shifted after repeated drug exposure. Exposure to a range of drugs of abuse leads to the type of relationship represented in this graph. The ordinate represents the bar‐pressing frequency of a rat that has a stimulating electrode placed in a reward area of the brain. In the plot obtained from the naive rat, bar‐pressing is relatively stable over time, suggesting that the animal is maintaining a level of reward around a stable set‐point. During withdrawal, the frequency of bar‐pressing is significantly increased initially, suggesting that more brain stimulation is necessary to ‘satisfy’ the animal. This has been referred to as a shift in the ‘hedonic set‐point’. Over time, the reward threshold returns to levels seen before drug exposure.


Further Reading

Koob GF (2008) A role for brain stress systems in addiction. Neuron 59: 11–34.

Pietrzykowski AZ, Friesen RM, Martin GE et al. (2008) Posttranscriptional regulation of BK channel splice variant stability by miR‐9 underlies neuroadaptation to alcohol. Neuron 59: 274–287.

Renthal W and Nestler EJ (2008) Epigenetic mechanisms in drug addiction. Trends in Molecular Medicine 14(8): 341–350.

Treistman SN, Chu B and Dopico A (1999) Molecular targets underlying ethanol‐mediated reduction of hormone release from neurohypophysial nerve terminals. In: Liu Y and Hunt W (eds) The Drunken Synapse, pp. 27–38. New York: Plenum Press.

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How to Cite close
Treistman, Steven N(Mar 2009) Addiction. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0000003.pub2]