동기부여 편의성

Motivational salience
참고 항목: 유익성(신경과학)

동기적 만족은 인지 과정이며 특정 대상, 인지된 사건 또는 결과로부터 개인의 행동을 동기를 부여하거나 멀어지게 하는 주의의 한 형태다.[1] 동기적 만족도는 특정 목표의 달성을 촉진하는 행동의 강도, 개인이 특정 목표를 달성하기 위해 소비할 시간과 에너지의 양, 그리고 특정 목표를 달성하기 위해 일하는 동안 개인이 기꺼이 받아들이려는 위험의 양을 조절한다.[1]

동기적 만족도는 특정 자극에 상대적인 개인의 행동에 대한 매력적이거나 혐오적인 효과에 의해 정의되는 두 가지 요소 과정으로 구성된다: 인센티브 만족도와 혐오적 만족이다.[1] 인센티브 만족도는 접근 행동을 유발하는 동기 부여 만족도의 매력적인 형태로서 운영자 강화, 바람직한 결과 및 즐거운 자극과 관련이 있다.[2][3] 혐오적 쾌감은 회피 행동을 유발하는 동기적 쾌감의 반동적 형태로서, 운영자 처벌, 바람직하지 않은 결과, 불쾌한 자극과 관련이 있다.[4]

인센티브 만족도

중독 및 의존 용어집[5][6][7][8]
  • 중독 – 상당한 위해와 부정적인 결과에도 불구하고 지속적으로 약물(알코올 포함)을 사용하는 것이 특징인 조직사회 장애
  • 중독성 약물 – 반복적으로 사용하는 정신 활성 물질은 뇌 보상 시스템에 미치는 약의 효과로 인해 훨씬 더 높은 비율의 물질 사용 장애와 관련이 있다.
  • 의존성 – 자극에 반복적으로 노출되는 것을 중단했을 때 철수 증후군과 관련된 적응 상태(예: 약물 섭취)
  • 약물 감작성 또는 역내성 – 주어진 용량에서 반복 투여로 인한 약물의 증가 효과
  • 약물 회수 – 반복적인 약물 사용 중단 시 발생하는 증상
  • 신체적 의존 – 지속적인 신체적-신체적 철수 증상(예: 피로 및 망상 떨림)을 수반하는 의존성
  • 심리적 의존 – 정서적-정신적 금단 증상(예: 이상증 및 무쾌감증)을 수반하는 의존성
  • 강화 자극 - 반복 행동의 반복 가능성을 증가시키는 자극
  • 보람 있는 자극 – 뇌가 본질적으로 긍정적이고 바람직한 것으로 해석하거나 접근할 수 있는 것으로 해석하는 자극
  • 감작성 – 반복적인 노출로 인한 자극에 대한 증폭된 반응
  • 물질 사용 장애 – 물질의 사용이 임상적으로 그리고 기능적으로 중대한 손상 또는 고통으로 이어지는 상태
  • 내성 – 주어진 용량에서 반복 투여로 인한 약물의 감소 효과

인센티브 만족은 동기적 요소를 포함하는 "욕망" 또는 "원하는" 속성을 보람 있는 자극에 혼동하는 인지 과정이다.[1][2][3][9] 보상은 식욕적인 행동(접근 행동이라고도 함)과 소모적인 행동을 유도하는 자극의 매력적이고 동기부여적인 성질이다.[3] "애호"의 의미가 즉시 읽을 가치가 있는 자극의 획득이나 소비에서 얻은 것은 좋아하는 쾌락에 유인적 현저성의" 원하는" 다르고,[9][10]유인적 현저성의" 원하는"는고 매력적인 바람직한 목표, transformi을 만드는 보람 있는 경기 부양책"동기 자석"품질을 제공한다.그것 ng 단순한 감각 경험에서 주의를 명령하고, 접근을 유도하고, 그것을 찾도록 하는 무언가에 이르기까지.[9][10]

인센티브 만족도는 많은 뇌 구조에 의해 조절되지만, 그것은 핵으로 알려진 복측 선조체 영역에 의해 자극에 할당된다.[1][2][9] 인센티브 만족도는 주로 도파민 신경전달에 의해 조절되지만,[note 1] 다른 도파민 경로와 쾌락적 핫스팟(예: 복측 팔리덤)에서의 활동도 인센티브 만족도를 조절한다.[2][9][10][11]

임상적 유의성

추가 정보: Pavlovian 악기 전달 § 임상적 중요성

중독

추가 정보: 중독 § 보상감각

자극에 대한 자극에 대한 인센티브의 배정은 중독에서 조절이 잘못된다.[1][9][10][12] 중독성 있는 약물은 본질적으로 보람이 있으며(즐거움과 혼동되지 않음) 따라서 인센티브의 유익성이 부여된 지속적인 약물 사용에 대한 1차적인 긍정적 강화제의 역할을 한다.[3][9][10][12] 중독의 발전 과정에서, 그렇지 않으면 그리고 심지어non-rewarding 중립을 자극한 약물 섭취로 반복 조합 중독성 약물 사용(즉, 그러한 자극 함수에 마약 단서로 시작하)의 조건 긍정적인 강화 물로서 활동하기 전에는 중립적인 자극을 유발하는 연상 배움의 과정을 촉발시킨다.[9][10][12] 약물 사용에 대한 조건화된 긍정적인 강화제로서, 이러한 이전의 중립적 자극은 인센티브 만족도(욕망으로 나타나며), 때로는 보상 민감화로 인해 병리학적으로 높은 수준에서 할당되며, 이는 원래 짝을 이룬 1차 강화제(예:[9][10][12] 중독성 약물의 사용)로 이행될 수 있다. 따라서 개인이 한동안 약물 사용을 금기시하다가 이러한 약물 단서 중 하나를 발견하게 되면 관련 약물에 대한 갈망이 다시 나타날 수 있다. 예를 들어, 마약 방지 기관들은 이전에 마약 사용의 위험성을 보여주기 위한 시도로 마약 투약 사진이 있는 포스터를 사용했다. 그러나 이러한 포스터는 포스터에 묘사된 자극을 볼 때 재발을 유발하는 자극의 효과 때문에 더 이상 사용되지 않는다.[citation needed]

중독에서, 약이나 다른 자극의 "liking"(쾌락 또는 쾌락적 가치)은 인센티브 만족의 감작화로 인해 "욕망" (즉, 욕망 또는 갈망)과 분리된다.[13] 실제로 약물 복용과 관련된 인센티브 만족도가 병리학적으로 증폭되면, 사용자는 약의 즐거운 효과에 대한 내성이 발달함에 따라 점점 덜 좋아하면서도 점점 더 약물을 원할 수 있다.[10]

신경정신병리학

도파민성 신경안정제

암페타민은 업무 편의성(업무 수행 동기를 부여)을 향상시키고 각성(깨끗함)을 증가시켜 결과적으로 목표 지향적인 행동을 촉진한다.[14][15][16] 암페타민의 강화와 동기부여 만족 촉진 효과는 대부분 중음부 경로에서 도파민 활성이 강화되었기 때문이다.[14]

참고 항목

메모들

  1. ^ 중격동 투영은 복측 티그먼트 영역과 측두엽 및 전두엽 피질을 연결하는 도파민 경로의 그룹이다.

참조

  1. ^ 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).
  2. ^ 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.
  3. ^ 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.
  4. ^ Koob GF, Moal ML (2006). Neurobiology of Addiction. Amsterdam: Elsevier/Academic Press. p. 415. ISBN 9780080497372.
  5. ^ 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.
  6. ^ 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.
  7. ^ "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. Retrieved 9 February 2015.
  8. ^ 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.
  9. ^ 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.
  10. ^ 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).
  11. ^ 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.
  12. ^ a b c d Edwards S (2016). "Reinforcement principles for addiction medicine; from recreational drug use to psychiatric disorder". Prog. Brain Res. Progress in Brain Research. 223: 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).
  13. ^ 베리지, K.C., 로빈슨, T.E. 보상에 있어서 도파민의 역할은 무엇인가: 쾌락적 영향, 보상 학습 또는 장려 편의? 두뇌 자원 두뇌 자원 1998년 12월 28일:309–69.
  14. ^ 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.
  15. ^ 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.
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