Motivational salience
(Redirected from Aversive salience)
Motivational salience is a cognitive process and a form of attention that motivates or propels an individual's behavior towards or away from a particular object, perceived event or outcome.[1] Motivational salience regulates the intensity of behaviors that facilitate the attainment of a particular goal, the amount of time and energy that an individual is willing to expend to attain a particular goal, and the amount of risk that an individual is willing to accept while working to attain a particular goal.[1]
Motivational salience is composed of two component processes that are defined by their attractive or aversive effects on an individual's behavior relative to a particular stimulus: incentive salience and aversive salience.[1] Incentive salience is the attractive form of motivational salience that causes approach behavior, and is associated with operant reinforcement, desirable outcomes, and pleasurable stimuli.[2][3] Aversive salience (sometimes known as fearful salience[4]) is the aversive form of motivational salience that causes avoidance behavior, and is associated with operant punishment, undesirable outcomes, and unpleasant stimuli.[5]
Incentive salience
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Incentive salience is a cognitive process that grants a "desire" or "want" attribute, which includes a motivational component to a rewarding stimulus.[1][2][3][9] Reward is the attractive and motivational property of a stimulus that induces appetitive behavior – also known as approach behavior – and consummatory behavior.[3] The "wanting" of incentive salience differs from "liking" in the sense that liking is the pleasure that is immediately gained from the acquisition or consumption of a rewarding stimulus;[9][10] the "wanting" of incentive salience serves a "motivational magnet" quality of a rewarding 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.[9][10]
Incentive salience is regulated by a number of brain structures, but it is assigned to stimuli by a region of the ventral striatum known as the nucleus accumbens shell.[1][2][9] Incentive salience is primarily regulated by dopamine neurotransmission in the mesocorticolimbic projection,[note 1] but activity in other dopaminergic pathways and hedonic hotspots (e.g., the ventral pallidum) also modulate incentive salience.[2][9][10][11]
Clinical significance
[edit]Addiction
[edit]The assignment of incentive salience to stimuli is dysregulated in addiction.[1][9][10][12] Addictive drugs are intrinsically rewarding (not to be confused with pleasure) and therefore function as primary positive reinforcers of continued drug use that are assigned incentive salience.[3][9][10][12] 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 act as conditioned positive reinforcers of addictive drug use (i.e., these stimuli start to function as drug cues).[9][10][12] As conditioned positive reinforcers of drug use, these previously neutral stimuli are assigned incentive salience (which manifests as a craving) – sometimes at pathologically high levels due to reward sensitization – which can transfer to the primary reinforcer (e.g., the use of an addictive drug) with which it was originally paired.[9][10][12] Thus, if an individual remains abstinent from drug use for some time and encounters one of these drug cues, a craving for the associated 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.[citation needed]
In addiction, the "liking" (pleasure or hedonic value) of a drug or other stimulus becomes dissociated from "wanting" (i.e., desire or craving) due to the sensitization of incentive salience.[13] 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.[10]
Neuropsychopharmacology
[edit]Dopaminergic psychostimulants
[edit]Amphetamine improves task saliency (motivation to perform a task) and increases arousal (wakefulness), in turn promoting goal-directed behavior.[14][15][16] The reinforcing and motivational salience-promoting effects of amphetamine are mostly due to enhanced dopaminergic activity in the mesolimbic pathway.[14]
See also
[edit]Notes
[edit]- ^ The mesocorticolimbic projection is a group of dopamine pathways that connects the ventral tegmental area to the nucleus accumbens and prefrontal cortex.
References
[edit]- ^ a b c d e f Puglisi-Allegra S, Ventura R (June 2012). "Prefrontal/accumbal catecholamine system processes high motivational salience". Front. Behav. Neurosci. 6: 31. doi:10.3389/fnbeh.2012.00031. PMC 3384081. PMID 22754514.
Motivational salience regulates the strength of goal seeking, the amount of risk taken and the energy invested from mild to extreme. ... Motivation can be conceptually described as a continuum along which stimuli can either reinforce or punish responses to other stimuli. Behaviorally, stimuli that reinforce are called rewarding and those that punish aversive (Skinner, 1953). Reward and aversion describe the impact a stimulus has on behavior, and provided of motivational properties, thus able to induce attribution of motivational salience. ... Attribution of motivational salience is related to the salience of an UCS (Dallman et al., 2003; Pecina et al., 2006). Thus, the more salient an UCS the more likely a neutral (to-be-conditioned) stimulus will be associated with it through motivational salience attribution. Prior experience is a major determinant of the motivational impact of any given stimulus (Borsook et al., 2007) and emotional arousal induced by motivational stimuli increases the attention given to stimuli influencing both the initial perceptual encoding and the consolidation process (Anderson et al., 2006; McGaugh, 2006).
- ^ a b c d 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. - ^ a b c d Schultz W (2015). "Neuronal reward and decision signals: from theories to data". Physiological Reviews. 95 (3): 853–951. doi:10.1152/physrev.00023.2014. PMC 4491543. PMID 26109341.
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.
- ^ Berridge, Kent (2019). "12: A Liking Versus Wanting Perspective on Emotion and the Brain". In Gruber, June (ed.). The Oxford Handbook of Positive Emotion and Psychopathology. Oxford/New York: Oxford University Press. p. 184.
- ^ Koob GF, Moal ML (2006). Neurobiology of Addiction. Amsterdam: Elsevier/Academic Press. p. 415. ISBN 9780080497372.
- ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–375. ISBN 9780071481274.
- ^ Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues in Clinical Neuroscience. 15 (4): 431–443. PMC 3898681. PMID 24459410.
Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.
- ^ Volkow ND, Koob GF, McLellan AT (January 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". New England Journal of Medicine. 374 (4): 363–371. doi:10.1056/NEJMra1511480. PMC 6135257. PMID 26816013.
Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder. - ^ a b c d e f g h i Berridge KC (April 2012). "From prediction error to incentive salience: mesolimbic computation of reward motivation". Eur. J. Neurosci. 35 (7): 1124–1143. doi:10.1111/j.1460-9568.2012.07990.x. PMC 3325516. PMID 22487042.
Here I discuss how mesocorticolimbic mechanisms generate the motivation component of incentive salience. Incentive salience takes Pavlovian learning and memory as one input and as an equally important input takes neurobiological state factors (e.g. drug states, appetite states, satiety states) that can vary independently of learning. Neurobiological state changes can produce unlearned fluctuations or even reversals in the ability of a previously learned reward cue to trigger motivation. Such fluctuations in cue-triggered motivation can dramatically depart from all previously learned values about the associated reward outcome. ... Associative learning and prediction are important contributors to motivation for rewards. Learning gives incentive value to arbitrary cues such as a Pavlovian conditioned stimulus (CS) that is associated with a reward (unconditioned stimulus or UCS). Learned cues for reward are often potent triggers of desires. For example, learned cues can trigger normal appetites in everyone, and can sometimes trigger compulsive urges and relapse in addicts. ... A brief CS encounter (or brief UCS encounter) often primes a pulse of elevated motivation to obtain and consume more reward UCS. This is a signature feature of incentive salience. ... When a Pavlovian CS+ is attributed with incentive salience it not only triggers 'wanting' for its UCS, but often the cue itself becomes highly attractive – even to an irrational degree. This cue attraction is another signature feature of incentive salience. ... An attractive CS often elicits behavioral motivated approach, and sometimes an individual may even attempt to 'consume' the CS somewhat as its UCS (e.g., eat, drink, smoke, have sex with, take as drug). 'Wanting' of a CS can turn also turn the formerly neutral stimulus into an instrumental conditioned reinforcer, so that an individual will work to obtain the cue (however, there exist alternative psychological mechanisms for conditioned reinforcement too). ... Two recognizable features of incentive salience are often visible that can be used in neuroscience experiments: (i) UCS-directed 'wanting' – CS-triggered pulses of intensified 'wanting' for the UCS reward; and (ii) CS-directed 'wanting' – motivated attraction to the Pavlovian cue, which makes the arbitrary CS stimulus into a motivational magnet.
- ^ a b c d e f g h Berridge KC, Kringelbach ML (May 2015). "Pleasure systems in the brain". Neuron. 86 (3): 646–664. doi:10.1016/j.neuron.2015.02.018. PMC 4425246. PMID 25950633.
An important goal in future for addiction neuroscience is to understand how intense motivation becomes narrowly focused on a particular target. Addiction has been suggested to be partly due to excessive incentive salience produced by sensitized or hyper-reactive dopamine systems that produce intense 'wanting' (Robinson and Berridge, 1993). But why one target becomes more 'wanted' than all others has not been fully explained. In addicts or agonist-stimulated patients, the repetition of dopamine-stimulation of incentive salience becomes attributed to particular individualized pursuits, such as taking the addictive drug or the particular compulsions. In Pavlovian reward situations, some cues for reward become more 'wanted' more than others as powerful motivational magnets, in ways that differ across individuals (Robinson et al., 2014b; Saunders and Robinson, 2013). ... However, hedonic effects might well change over time. As a drug was taken repeatedly, mesolimbic dopaminergic sensitization could consequently occur in susceptible individuals to amplify 'wanting' (Leyton and Vezina, 2013; Lodge and Grace, 2011; Wolf and Ferrario, 2010), even if opioid hedonic mechanisms underwent down-regulation due to continual drug stimulation, producing 'liking' tolerance. Incentive-sensitization would produce addiction, by selectively magnifying cue-triggered 'wanting' to take the drug again, and so powerfully cause motivation even if the drug became less pleasant (Robinson and Berridge, 1993).
- ^ Berridge, Kent C.; O’Doherty, John P. (1 January 2014). Fehr, Paul W. GlimcherErnst (ed.). Chapter 18 – From Experienced Utility to Decision Utility. San Diego: Academic Press. pp. 335–351. doi:10.1016/B978-0-12-416008-8.00018-8. ISBN 978-0-12-416008-8.
- ^ a b c d Edwards S (2016). "Reinforcement principles for addiction medicine; from recreational drug use to psychiatric disorder". Neuroscience for Addiction Medicine: From Prevention to Rehabilitation - Constructs and Drugs. Progress in Brain Research. Vol. 223. pp. 63–76. doi:10.1016/bs.pbr.2015.07.005. ISBN 9780444635457. PMID 26806771.
Abused substances (ranging from alcohol to psychostimulants) are initially ingested at regular occasions according to their positive reinforcing properties. Importantly, repeated exposure to rewarding substances sets off a chain of secondary reinforcing events, whereby cues and contexts associated with drug use may themselves become reinforcing and thereby contribute to the continued use and possible abuse of the substance(s) of choice. ...
An important dimension of reinforcement highly relevant to the addiction process (and particularly relapse) is secondary reinforcement (Stewart, 1992). Secondary reinforcers (in many cases also considered conditioned reinforcers) likely drive the majority of reinforcement processes in humans. In the specific case of drug [addiction], cues and contexts that are intimately and repeatedly associated with drug use will often themselves become reinforcing ... A fundamental piece of Robinson and Berridge's incentive-sensitization theory of addiction posits that the incentive value or attractive nature of such secondary reinforcement processes, in addition to the primary reinforcers themselves, may persist and even become sensitized over time in league with the development of drug addiction (Robinson and Berridge, 1993). ...
Negative reinforcement is a special condition associated with a strengthening of behavioral responses that terminate some ongoing (presumably aversive) stimulus. In this case we can define a negative reinforcer as a motivational stimulus that strengthens such an "escape" response. Historically, in relation to drug addiction, this phenomenon has been consistently observed in humans whereby drugs of abuse are self-administered to quench a motivational need in the state of withdrawal (Wikler, 1952).{{cite book}}:|journal=ignored (help) - ^ 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.
- ^ a b Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York, USA: McGraw-Hill Medical. pp. 318, 321. ISBN 9780071481274.
Therapeutic (relatively low) doses of psychostimulants, such as methylphenidate and amphetamine, improve performance on working memory tasks both in normal subjects and those with ADHD. ... stimulants act not only on working memory function, but also on general levels of arousal and, within the nucleus accumbens, improve the saliency of tasks. Thus, stimulants improve performance on effortful but tedious tasks ... through indirect stimulation of dopamine and norepinephrine receptors. ...
Beyond these general permissive effects, dopamine (acting via D1 receptors) and norepinephrine (acting at several receptors) can, at optimal levels, enhance working memory and aspects of attention. - ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 10: Neural and Neuroendocrine Control of the Internal Milieu". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York, USA: McGraw-Hill Medical. p. 266. ISBN 9780071481274.
Dopamine acts in the nucleus accumbens to attach motivational significance to stimuli associated with reward.
- ^ Wood S, Sage JR, Shuman T, Anagnostaras SG (January 2014). "Psychostimulants and cognition: a continuum of behavioral and cognitive activation". Pharmacol. Rev. 66 (1): 193–221. doi:10.1124/pr.112.007054. PMC 3880463. PMID 24344115.
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