A reward or reinforcement is something that, when presented after a behavior, causes that behavior to increase in intensity and/or frequency. Certain neural structures, called the reward system are critically involved mediating the effects of reward. [1]

Drugs of abuse target the brain's pleasure center.[1]

Reward as a behavioral effect

Reward or reinforcement is an objective way to describe the positive value an individual ascribes to an object, behavioral act or an internal physical state. Primary rewards include those that are necessary for the survival of species, such as food, sexual contact, or successful aggression.[2]

Secondary rewards derive their value from primary rewards. Money is a good example. They can be produced experimentally by pairing a neutral stimulus with a known reward. Things such as pleasurable touch and beautiful music are often said to be secondary rewards, but such claims are questionable. For example, there is a good deal of evidence that physical contact, as in cuddling and grooming, is an unlearned or primary reward [3]. Rewards are generally considered more desirable than punishment in modifying behavior.[4]

Discovery of the reward system

Skinner box

In a fundamental discovery made in 1954, researchers James Olds and Peter Milner found that low-voltage electrical stimulation of certain regions of the brain of the rat acted as a reward in teaching the animals to run mazes and solve problems.[5][6] It seemed that stimulation of those parts of the brain gave the animals pleasure, [5] and in later work humans reported pleasurable sensations from such stimulation. When rats were tested in Skinner boxes where they could stimulate the reward system by pressing a lever, the rats pressed for hours at a rate up to 2000 times per hour.[6] Research in the next two decades established that dopamine is one of the main chemicals aiding neural signaling in these regions, and dopamine was suggested to be the brain’s “pleasure chemical.”[7]

Anatomy of the reward system

The major neurochemical pathway of the reward system in the brain involves the mesolimbic and mesocortical pathway. Of these pathways, the mesolimbic pathway plays the major role, and goes from the ventral tegmental area via the medial forebrain bundle to nucleus accumbens, which is the primary release site for the neurotransmitter dopamine. Dopamine acts on D1 or D2 receptors to either stimulate (D1) or inhibit (D2) the production of cAMP.

Modulation by drugs

Main article: Drug addiction

Almost all drugs causing drug addiction increase the dopamine release in the mesolimbic pathway[8], e.g. opioids, nicotine, amphetamine, ethanol and cocaine. After prolonged use, psychological drug tolerance and sensitization arises.

Psychological drug tolerance

The reward system is partly responsible for the psychological part of drug tolerance. One explanation of this is a sustained activation of the CREB protein, causing a larger dose to be needed to reach the same effect.


Sensitization is an increase in the user's sensitivity to the effects of the substance, counter to the effects of CREB. A transcription factor, known as delta FosB, is thought to be involved by activating genes that causes sensitization. The hypersensitivity that it causes is thought to be responsible for the intense cravings associated with drug addiction, and is often extended to even the peripheral cues of drug use, such as related behaviors or the sight of drug paraphernalia.

See also


  1. ^ a b "Drugs, Brains, and Behavior: The Science of Addiction".
  2. ^ "Dopamine Involved In Aggression". Medical News Today. 2008-01-15. Retrieved 2010-11-14.
  3. ^ Harlow, H. F. (1958) The nature of love. American Psychologist, 13, 679-685
  4. ^ "Smacking children 'does not work'". BBC News. 1999-01-11. Retrieved 2010-05-22.
  5. ^ a b "human nervous system".
  6. ^ a b "Positive Reinforcement Produced by Electrical Stimulation of Septal Area and Other Regions of Rat Brain".
  7. ^ "The Functional Neuroanatomy of Pleasure and Happiness".
  8. ^ Rang, H. P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. p. 596. ISBN 0-443-07145-4.