Incentive salience

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Addiction and dependence glossary[1][2][3][4]
addiction – a medical condition characterized by compulsive engagement in rewarding stimuli despite adverse consequences
addictive behavior – a behavior that is both rewarding and reinforcing
addictive drug – a drug that is both rewarding and reinforcing
dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake)
drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose
drug withdrawal – symptoms that occur upon cessation of repeated drug use
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)
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
sensitization – an amplified response to a stimulus resulting from repeated exposure to it
substance use disorder - a condition in which the use of substances leads to clinically and functionally significant impairment or distress
tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose
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Incentive salience refers to the "wanting" or "desire" attribute given by the brain – specifically, by the nucleus accumbens shell – to a rewarding stimulus.[5][6] Reward is the attractive and motivational property of a stimulus that induces appetitive behavior – also known as approach behavior – and consummatory behavior.[6] This "wanting" is unlike "liking" in that liking is a pleasure immediately gained from consumption or other contact with stimuli, while the "wanting" of incentive salience is a motivational magnet quality of a stimulus that makes it a desirable and attractive goal, transforming it from a mere sensory experience into something that commands attention, induces approach, and causes it to be sought out. Incentive salience is regulated by dopamine activity in the mesocorticolimbic pathway of the brain.[5][7]

The assignment of incentive salience to stimuli is dysregulated in addiction. During the development of an addiction, the repeated association of otherwise neutral and even non-rewarding stimuli with drug consumption triggers an associative learning process that causes these previously neutral stimuli to become secondary reinforcers of addictive drug use. As secondary reinforcers of drug use, these previously neutral stimuli are assigned incentive salience (which manifests as a craving), sometimes at pathologically high levels, which transfers to the primary reinforcer (i.e., the use of an addictive drug) with which it was originally paired. Thus, if a person's addiction subsides and the individual subsequently encounters one of these secondary reinforcers, a craving for that drug may reappear. For example, anti-drug agencies previously used posters with images of drug paraphernalia as an attempt to show the dangers of drug use. However, such posters are no longer used because of the effects of incentive salience in causing relapse upon sight of the stimuli illustrated in the posters.

In addiction, the "liking" (pleasure or hedonic value) of a drug or other stimulus becomes dissociated from the "wanting" (level of desire for) attribute due to the sensitization of incentive salience.[8] In fact, if the incentive salience associated with drug-taking becomes pathologically amplified, the user may want the drug more and more while liking it less and less as tolerance develops to the drug's pleasurable effects.

Incentive salience is the form of motivational salience that is associated with reward (an attractive phenomenon), as opposed to punishment (an avoidance phenomenon).[5][6]

See also[edit]

References[edit]

  1. ^ 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. 
  2. ^ Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. 15 (4): 431–443. PMC 3898681free to read. PMID 24459410. 
  3. ^ "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. Retrieved 9 February 2015. 
  4. ^ Volkow ND, Koob GF, McLellan AT (January 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". N. Engl. J. Med. 374 (4): 363–371. doi:10.1056/NEJMra1511480. PMID 26816013. 
  5. ^ a b c Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY, eds. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 147–148, 367, 376. ISBN 978-0-07-148127-4. VTA DA neurons play a critical role in motivation, reward-related behavior (Chapter 15), attention, and multiple forms of memory. This organization of the DA system, wide projection from a limited number of cell bodies, permits coordinated responses to potent new rewards. Thus, acting in diverse terminal fields, dopamine confers motivational salience (“wanting”) on the reward itself or associated cues (nucleus accumbens shell region), updates the value placed on different goals in light of this new experience (orbital prefrontal cortex), helps consolidate multiple forms of memory (amygdala and hippocampus), and encodes new motor programs that will facilitate obtaining this reward in the future (nucleus accumbens core region and dorsal striatum). In this example, dopamine modulates the processing of sensorimotor information in diverse neural circuits to maximize the ability of the organism to obtain future rewards. ...
    The brain reward circuitry that is targeted by addictive drugs normally mediates the pleasure and strengthening of behaviors associated with natural reinforcers, such as food, water, and sexual contact. Dopamine neurons in the VTA are activated by food and water, and dopamine release in the NAc is stimulated by the presence of natural reinforcers, such as food, water, or a sexual partner. ...
    The NAc and VTA are central components of the circuitry underlying reward and memory of reward. As previously mentioned, the activity of dopaminergic neurons in the VTA appears to be linked to reward prediction. The NAc is involved in learning associated with reinforcement and the modulation of motoric responses to stimuli that satisfy internal homeostatic needs. The shell of the NAc appears to be particularly important to initial drug actions within reward circuitry; addictive drugs appear to have a greater effect on dopamine release in the shell than in the core of the NAc.
     
  6. ^ a b c Schultz W (2015). "Neuronal reward and decision signals: from theories to data" (PDF). Physiological Reviews. 95 (3): 853–951. doi:10.1152/physrev.00023.2014. Archived from the original (PDF) on 6 September 2015. Retrieved 24 September 2015. Rewards in operant conditioning are positive reinforcers. ... Operant behavior gives a good definition for rewards. Anything that makes an individual come back for more is a positive reinforcer and therefore a reward. Although it provides a good definition, positive reinforcement is only one of several reward functions. ... Rewards are attractive. They are motivating and make us exert an effort. ... Rewards induce approach behavior, also called appetitive or preparatory behavior, and consummatory behavior. ... Thus any stimulus, object, event, activity, or situation that has the potential to make us approach and consume it is by definition a reward. ... Rewarding stimuli, objects, events, situations, and activities consist of several major components. First, rewards have basic sensory components (visual, auditory, somatosensory, gustatory, and olfactory) ... Second, rewards are salient and thus elicit attention, which are manifested as orienting responses (FIGURE 1, middle). The salience of rewards derives from three principal factors, namely, their physical intensity and impact (physical salience), their novelty and surprise (novelty/surprise salience), and their general motivational impact shared with punishers (motivational salience). A separate form not included in this scheme, incentive salience, primarily addresses dopamine function in addiction and refers only to approach behavior (as opposed to learning) ... Third, rewards have a value component that determines the positively motivating effects of rewards and is not contained in, nor explained by, the sensory and attentional components (FIGURE 1, right). This component reflects behavioral preferences and thus is subjective and only partially determined by physical parameters. Only this component constitutes what we understand as a reward. It mediates the specific behavioral reinforcing, approach generating, and emotional effects of rewards that are crucial for the organism’s survival and reproduction, whereas all other components are only supportive of these functions. ... These emotions are also called liking (for pleasure) and wanting (for desire) in addiction research (471) and strongly support the learning and approach generating functions of reward. 
  7. ^ Berridge, Kent C.; O’Doherty, John P. (2014-01-01). Fehr, Paul W. GlimcherErnst, ed. Chapter 18 - From Experienced Utility to Decision Utility. San Diego: Academic Press. pp. 335–351. ISBN 978-0-12-416008-8. 
  8. ^ Berridge, K.C., Robinson, T.E. What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience? Brain Res Brain Res Rev. 1998 Dec; 28(3):309–69.