Reward system
Certain neural structures, called the reward system, are critically involved in mediating the effects of reinforcement. A reward is an appetitive stimulus given to a human or some other animal to alter its behavior. Rewards typically serve as reinforcers. A reinforcer is something that, when presented after a behavior, causes the probability of that behavior's occurrence to increase. Note that, just because something is labelled as a reward, it does not necessarily imply that it is a reinforcer. A reward can be defined as reinforcer only if its delivery increases the probability of a behavior.[1]
Reward or reinforcement is an objective way to describe the positive value that 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 and sexual contact.[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]
Definition
In neuroscience, the reward system is a collection of brain structures that attempts to regulate and control behavior by inducing pleasurable effects. It is a brain circuit that, when activated, reinforces behaviors. The circuit includes the dopamine-containing neurons of the ventral tegmental area, the nucleus accumbens, and part of the prefrontal cortex.[5]
History
James Olds and Peter Milner were researchers who found the reward system in 1954. They discovered, while trying to teach rats how to solve problems and run mazes, stimulation of certain regions of the brain. Where the stimulation was found seemed to give pleasure to the animals. They tried the same thing with humans and the results were similar.
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.[6][7] It seemed that stimulation of those parts of the brain gave the animals pleasure,[6] 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.[7] 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”.[8]
Anatomy of the reward system
The major neurochemical pathway of the reward system in the brain involves the mesolimbic and mesocortical pathways. Of these pathways, the mesolimbic pathway plays the major role, and goes from the ventral tegmental area (VTA) via the medial forebrain bundle to nucleus accumbens. The VTA 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.[citation needed]
Humans and animals seem to have a similar sense of pleasure.[9] However, pleasure is qualitatively and quantitatively different in humans than in animals.[citation needed] The human brain deciphers pleasant events and adds depth by changing the way humans pay attention and notice pleasures. The sense of pleasures differ in humans compared to animals because culture, life events, art, and other cognitive sources expand our understanding. This can make one realize how great a pleasure is or how displeasurable it may be.[10]
Animals vs humans
Based on data from Kent Berridge, the liking and disliking reaction involving taste shows similarities among human newborns, orangutans, and rats. Most neuroscience studies have shown that dopamine alterations change the level of likeliness toward a reward, which is called the hedonic impact. This is changed by how hard the reward is worked for. Experimenter Berridge modified testing a bit when working with reactions by recording the facial expressions of liking and disliking. Berridge discovered that by blocking dopamine systems there did not seem to be a change of the positive reaction to something sweet; in other words, the hedonic impact remained the same even with this change. It is believed that dopamine is the brain's main pleasure neurotransmitter but, with these results, that did not seem to be the case. Even with more intense dopamine alterations, the data seemed to remain the same. This is when Berridge came up with the incentive salience hypothesis to explain why the dopamine seems to only sometimes control pleasure when in fact that does not prove to be happening at all. This hypothesis dealt with the wanting aspect of rewards. Scientists can use this study done by Berridge to further explain the reasoning of getting such strong urges when addicted to drugs. Some addicts respond to certain stimuli involving neural changes caused by drugs. This sensitization in the brain is similar to the effect of dopamine because wanting and liking reactions occur. Human and animal brains and behaviors experience similar changes regarding reward systems because they both are so prominent.[9]
Modulation by drugs
Almost all drugs causing drug addiction increase the dopamine release in the mesolimbic pathway,[11] e.g. opioids, nicotine, amphetamine, ethanol, and cocaine. After prolonged use, psychological drug tolerance and sensitization arises.[citation needed] Drugs have many different effects on the brain; however, they all follow the same path. They stimulate the brain in various ways to receive a reward or, in this case, a high. The relationship between drugs and the reward system is rather close. Drugs provide an almost-immediate reward that often leads to addiction. For example, one drinks alcohol to feel intoxicated. This would be considered to be positive reinforcement. On the other hand, if one were to quit after long periods of binge drinking, there is a strong possibility of alcohol withdrawal symptoms. This would be identified as negative reinforcement. In “Neurobiology of alcohol dependence: focus on motivational mechanisms,” Gilpin states that the path from positive to negative reinforcement is taken as a drug's impact on the brain moves from abuse to dependence.
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.[citation needed]
Sensitization
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.[12]
Neurotransmitters and reward circuits
Dopamine is one of the primary neurotransmitters involved in drug consumption and addiction. Dopamine receptors are stimulated while someone is consuming a drug or when the thought of doing a drug occurs. In fact, decreases in dopamine levels occur during the withdrawal stage of quitting a drug like cocaine or alcohol. Serotonin is another neurotransmitter targeted by drugs. Endorphins are another type of neurotransmitter targeted by drugs. Endorphins are related to pain, fear, sex, and drugs. Certain drugs stimulate serotonin and endorphin receptors, which creates a type of euphoria. Neurotransmitters such as these play a major role in the reward systems of the brain. However, the manipulation of these neurotransmitters can have adverse affects on a human being. The continued use of drugs can cause degeneration of such neurotransmitters causing personality disorders and prolonged personality changes in an individual.
See also
- Anterior cingulate cortex#Reward based learning theory
- Classical conditioning
- Operant conditioning
- Brain stimulation reward
- Drug addiction#Reward circuit
- Reinforcer
- Decision making
- Motivation
- Addiction
- Psychoactive drug
- Ventral tegmentum#Reward system
- Incentive salience
- Pleasure center
- Learned industriousness
References
- ↑ 1.0 1.1 "Drugs, Brains, and Behavior: The Science of Addiction". drugabuse.gov.
- ↑ "Dopamine Involved In Aggression". Medical News Today. 2008-01-15. Retrieved 2010-11-14.
- ↑ Harlow, H. F. (1958) The nature of love. American Psychologist, 13, 679-685
- ↑ "Smacking children 'does not work'". BBC News. 1999-01-11. Retrieved 2010-05-22.
- ↑ "Associated Behavioral Health".
- ↑ 6.0 6.1 "human nervous system".
- ↑ 7.0 7.1 "Positive Reinforcement Produced by Electrical Stimulation of Septal Area and Other Regions of Rat Brain".
- ↑ "The Functional Neuroanatomy of Pleasure and Happiness".
- ↑ 9.0 9.1 Berridge, Kent. "Affective neuroscience of pleasure: reward in humans and animals". Retrieved 20 October 2012.
- ↑ Bear, Mark (2006). Neuroscience. Library of Congress Cataloging. pp. 522–525. ISBN 0-7817-6003-8.
- ↑ Rang, H. P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. p. 596. ISBN 0-443-07145-4.
- ↑ Robinson TE & Berridge KC (1993). "The neural basis of drug craving: an incentive-sensitization theory of addiction". Brain Research Reviews 18 (3): 247–91. PMID 8401595.
External links
Wikimedia Commons has media related to Reward system. |