Reward system

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Drugs of abuse target the brain's pleasure center.[1]
Addiction glossary[2][3][4]
addiction – a state characterized by compulsive engagement in rewarding stimuli despite adverse consequences
reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them
rewarding stimuli – stimuli that the brain interprets as intrinsically positive or as something to be approached
addictive drug – a drug that is both rewarding and reinforcing
addictive behavior – a behavior that is both rewarding and reinforcing
sensitization – an amplified response to a stimulus resulting from repeated exposure to it
drug tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose
drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose
dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake)
physical dependence – dependence that involves persistent physical–somatic withdrawal symptoms (e.g., fatigue and delirium tremens)
psychological dependence – dependence that involves emotional–motivational withdrawal symptoms (e.g., dysphoria and anhedonia)
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The reward system is a group of neural structures that 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.[5] 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.[6] Rewards are generally considered more desirable than punishment in modifying behavior.[7]

The brain structures which compose the reward system include the: ventral tegmental area, ventral striatum (specifically, the nucleus accumbens), dorsal striatum, prefrontal cortex, anterior cingulate cortex, insular cortex, hippocampus, hypothalamus, amygdala, and the remainder of the extended amygdala.[8][9]

Definition[edit]

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.[10]

Anatomy of the reward system[edit]

The basal ganglia circuit, specifically the mesolimbic pathway (ventral tegmental area and nucleus accumbens), is the center of the reward system yet there are more circuits and brain structures such as the anterior cingulate cortex, and midbrain dopamine pathways. The major neurochemical pathway of the reward system in the brain is the mesocorticolimbic pathway, which includes both the mesolimbic and mesocortical pathways. The ventral tegmental area (VTA) is a source of many dopamine pathways in the brain, which are neurons which use the neurotransmitter dopamine to transmit a signal to other structures. Dopamine acts on D1-like receptors or D2-like receptors to either stimulate (D1-like) or inhibit (D2-like) the production of cAMP.[11]

Humans and animals seem to have a similar sense of pleasure.[12] 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.[13]

Animals vs humans[edit]

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.[12]

History[edit]

Skinner box

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.[14][15] It seemed that stimulation of those parts of the brain gave the animals pleasure,[14] 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.[15] 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”.[16]

Ivan Pavlov was a psychologist who used the reward system in order to study classical training. Pavlov used the reward system by rewarding dogs with food after they had heard a bell or another stimulant. Pavlov was rewarding the dogs so that the dogs associated food, the reward, with the bell, the stimulant. [17] Edward L. Thorndike used the reward system in order to study operant conditioning. He began by putting cats in a puzzle box and placing food outside of the box so that the cat will want to escape. The cats worked to get out of the puzzle box to get to the food. Although the cats ate the food after they escaped the box, Thorndike learned that the cats attempted to escape the box without the reward of food. Thorndike used the rewards of food and freedom in order to stimulate the reward system of the cats. Thorndike used this in order to see how the cats learned to escape the box. [18]

The practices of reinforcement and punishment is effective due to the brain’s reward system. Reinforcements are stimulants that make a person more likely to do what is being promoted. A reinforcement is a stimulant that makes the person more likely to do what the reinforcement is promoting. The reward system categorizes reinforcements such as, money, food, and water; as positive rewards. The positive perception from the reward system then makes a person want to perform the action that produced the reinforcement. Punishments are the opposite of reinforcements. Punishment is when a stimulant is taken away for doing an act. The reward system systemizes punishments as the loss of a reward and now the person will not want to do the act that resulted in the reward being taken away. [19]

The mental disorder of depression is partially caused by the reward system. A person who is depressed has a less reactive reward system. Due to this reduced reward system, it leads to a depressed person who is unable to react to positive rewards that they receive. Because of the person’s inability to react to positive stimulants the person is unable to feel positive about anything. This pessimistic outlook on life causes the person dealing with depression to question their life and all the things that they own. The person does not consider rewards such as: life, a job, money, and family as rewards. The person's unreactive reward system causes no positivity in the person's life, and this leads the contemplation of suicide in order to escape such a life. [20]

Substance and behavioral addictions[edit]

Main article: ΔFosB

ΔFosB (delta FosB), a gene transcription factor, is the common factor among virtually all forms of addiction (behavioral addictions and drug addictions) that, when overexpressed in D1-type medium spiny neurons in the nucleus accumbens, is necessary and sufficient for many types of addiction-related plasticity; specifically, the overexpression of ΔFosB in the nucleus accumbens induces an addictive state and modulates many forms of behavioral and neural plasticity that occur in addiction. Examples of behavioral plasticity regulated by ΔFosB include drug self-administration, reward sensitization, and reward cross-sensitization effects among reinforcers. Examples of neuroplasticity modulated by ΔFosB include altered trafficking or density of NMDA receptors, AMPA receptors, and dopamine receptors in the striatum and nucleus accumbens.

Addictive drugs, and hence addictive behaviors, are rewarding and reinforcing (i.e., are addictive) due to their effects on the dopamine reward pathway.[9][21]

See also[edit]

References[edit]

  1. ^ a b "Drugs, Brains, and Behavior: The Science of Addiction". drugabuse.gov. 
  2. ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–375. ISBN 9780071481274. 
  3. ^ Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. 15 (4): 431–443. PMC 3898681. PMID 24459410. 
  4. ^ "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. Retrieved 9 February 2015. 
  5. ^ "Dopamine Involved In Aggression". Medical News Today. 15 January 2008. Retrieved 14 November 2010. 
  6. ^ Harlow, H. F. (1958) The nature of love. American Psychologist, 13, 679–685
  7. ^ "Smacking children 'does not work'". BBC News. 11 January 1999. Retrieved 22 May 2010. 
  8. ^ Grall-Bronnec M, Sauvaget A (2014). "The use of repetitive transcranial magnetic stimulation for modulating craving and addictive behaviours: a critical literature review of efficacy, technical and methodological considerations". Neurosci. Biobehav. Rev. 47: 592–613. doi:10.1016/j.neubiorev.2014.10.013. PMID 25454360. Studies have shown that cravings are underpinned by activation of the reward and motivation circuits (McBride et al., 2006, Wang et al., 2007, Wing et al., 2012, Goldman et al., 2013, Jansen et al., 2013 and Volkow et al., 2013). According to these authors, the main neural structures involved are: the nucleus accumbens, dorsal striatum, orbitofrontal cortex, anterior cingulate cortex, dorsolateral prefrontal cortex (DLPFC), amygdala, hippocampus and insula. 
  9. ^ a b Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disordersedition = 2nd". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience. New York: McGraw-Hill Medical. pp. 365–366, 376. ISBN 9780071481274. The neural substrates that underlie the perception of reward and the phenomenon of positive reinforcement are a set of interconnected forebrain structures called brain reward pathways; these include the nucleus accumbens (NAc; the major component of the ventral striatum), the basal forebrain (components of which have been termed the extended amygdala, as discussed later in this chapter), hippocampus, hypothalamus, and frontal regions of cerebral cortex. These structures receive rich dopaminergic innervation from the ventral tegmental area (VTA) of the midbrain. Addictive drugs are rewarding and reinforcing because they act in brain reward pathways to enhance either dopamine release or the effects of dopamine in the NAc or related structures, or because they produce effects similar to dopamine. ... A macrostructure postulated to integrate many of the functions of this circuit is described by some investigators as the extended amygdala. The extended amygdala is said to comprise several basal forebrain structures that share similar morphology, immunocytochemical features, and connectivity and that are well suited to mediating aspects of reward function; these include the bed nucleus of the stria terminalis, the central medial amygdala, the shell of the NAc, and the sublenticular substantia innominata. 
  10. ^ "Associated Behavioral Health". 
  11. ^ Trantham-Davidson, H., Neely, L. C., Lavin, A., & Seamans, J. K. (2004). Mechanisms underlying differential D1 versus D2 dopamine receptor regulation of inhibition in prefrontal cortex. The Journal of Neuroscience, 24(47), 10652–10659.
  12. ^ a b Berridge, Kent. "Affective neuroscience of pleasure: reward in humans and animals" (PDF). Retrieved 20 October 2012. 
  13. ^ Bear, Mark (2006). Neuroscience. Library of Congress Cataloging. pp. 522–525. ISBN 0-7817-6003-8. 
  14. ^ a b "human nervous system". 
  15. ^ a b "Positive Reinforcement Produced by Electrical Stimulation of Septal Area and Other Regions of Rat Brain". 
  16. ^ "The Functional Neuroanatomy of Pleasure and Happiness". 
  17. ^ https://books.google.com/books?hl=en&lr=&id=cknrYDqAClkC&oi=fnd&pg=PA1&dq=pavlov&ots=KApln9W8Kb&sig=brINTzKpYOHv_jftPXT1IZO2-ks#v=onepage&q=pavlov&f=false
  18. ^ Fridlund, Alan and James Kalat. Mind and Brain, the Science of Psychology. California: Cengage Learning, 2014. Print.
  19. ^ Fridlund, Alan and James Kalat. Mind and Brain, the Science of Psychology. California: Cengage Learning, 2014. Print.
  20. ^ http://www.sciencedirect.com/science/article/pii/S0278584601001567
  21. ^ Rang, H. P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. p. 596. ISBN 0-443-07145-4. 

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