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1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19  Schultz W (2015). "Neuronal reward and decision signals: from theories to data". Physiological Reviews. ج. 95 ع. 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. ... Rewards can also be intrinsic to behavior (31, 546, 547). They contrast with extrinsic rewards that provide motivation for behavior and constitute the essence of operant behavior in laboratory tests. Intrinsic rewards are activities that are pleasurable on their own and are undertaken for their own sake, without being the means for getting extrinsic rewards. ... Intrinsic rewards are genuine rewards in their own right, as they induce learning, approach, and pleasure, like perfectioning, playing, and enjoying the piano. Although they can serve to condition higher order rewards, they are not conditioned, higher order rewards, as attaining their reward properties does not require pairing with an unconditioned reward. ...  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.
1 2 3 4 5  Berridge KC، Kringelbach ML (مايو 2015). "Pleasure systems in the brain". Neuron. ج. 86 ع. 3: 646–664. DOI:10.1016/j.neuron.2015.02.018. PMC:4425246. PMID:25950633. In the prefrontal cortex, recent evidence indicates that the [orbitofrontal cortex] OFC and insula cortex may each contain their own additional hot spots (D.C. Castro et al., Soc. Neurosci., abstract). In specific subregions of each area, either opioid-stimulating or orexin-stimulating microinjections appear to enhance the number of liking reactions elicited by sweetness, similar to the [nucleus accumbens] NAc and [ventral pallidum] VP hot spots. Successful confirmation of hedonic hot spots in the OFC or insula would be important and possibly relevant to the orbitofrontal mid-anterior site mentioned earlier that especially tracks the subjective pleasure of foods in humans (Georgiadis et al., 2012; Kringelbach, 2005; Kringelbach et al., 2003; Small et al., 2001; Veldhuizen et al., 2010). Finally, in the brainstem, a hindbrain site near the parabrachial nucleus of dorsal pons also appears able to contribute to hedonic gains of function (Söderpalm and Berridge, 2000). A brainstem mechanism for pleasure may seem more surprising than forebrain hot spots to anyone who views the brainstem as merely reflexive, but the pontine parabrachial nucleus contributes to taste, pain, and many visceral sensations from the body and has also been suggested to play an important role in motivation (Wu et al., 2012) and in human emotion (especially related to the somatic marker hypothesis) (Damasio, 2010).
↑  "Dopamine Involved In Aggression". Medical News Today. 15 يناير 2008. مؤرشف من الأصل في 2010-09-23. اطلع عليه بتاريخ 2010-11-14.
↑  Malenka RC، Nestler EJ، Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (ط. 2nd). New York: McGraw-Hill Medical. ص. 364–375. ISBN:9780071481274.
↑  Nestler EJ (ديسمبر 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. ج. 15 ع. 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.
↑  "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. اطلع عليه بتاريخ 2015-02-09.
↑  Volkow ND، Koob GF، McLellan AT (يناير 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". N. Engl. J. Med. ج. 374 ع. 4: 363–371. DOI:10.1056/NEJMra1511480. 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.
1 2  Salamone JD، Correa M. "The Mysterious Motivational Functions of Mesolimbic Dopamine". Neuron. ج. 76 ع. 3: 470–485. DOI:10.1016/j.neuron.2012.10.021. PMC:4450094. PMID:23141060.
↑  Hyman، Steven E.؛ Malenka، Robert C.؛ Nestler، Eric J. (2006). "Neural mechanisms of addiction: the role of reward-related learning and memory". Annual Review of Neuroscience. ج. 29: 565–98. DOI:10.1146/annurev.neuro.29.051605.113009. PMID:16776597.
↑  Steiner، Heinz؛ Van Waes، Vincent (2013). "Addiction-related gene regulation: Risks of exposure to cognitive enhancers vs. Other psychostimulants". Progress in Neurobiology. ج. 100: 60–80. DOI:10.1016/j.pneurobio.2012.10.001. PMC:3525776. PMID:23085425.
↑  Wenzel، JM؛ Rauscher، NA؛ Cheer، JF؛ Oleson، EB (2015). "A role for phasic dopamine release within the nucleus accumbens in encoding aversion: a review of the neurochemical literature". ACS Chem Neurosci. ج. 6 ع. 1: 16–26. DOI:10.1021/cn500255p. PMID:25491156. {{استشهاد بدورية محكمة}}: الوسيط غير المعروف |name-list-format= تم تجاهله يقترح استخدام |name-list-style= (مساعدة)
1 2  
Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 10: Neural and Neuroendocrine Control of the Internal Milieu". في Sydor A, Brown RY (المحرر). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (ط. 2nd). New York: McGraw-Hill Medical. ص. 266. ISBN:978-0-07-148127-4. Dopamine acts in the nucleus accumbens to attach motivational significance to stimuli associated with reward.{{استشهاد بكتاب}}:  صيانة الاستشهاد: أسماء متعددة: قائمة المؤلفين (link)
↑  
Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (المحرر). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (ط. 2nd). New York: McGraw-Hill Medical. ص. 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.{{استشهاد بكتاب}}:  صيانة الاستشهاد: أسماء متعددة: قائمة المؤلفين (link)
1 2 3 4 5 6 7  Yager LM، Garcia AF، Wunsch AM، Ferguson SM (أغسطس 2015). "The ins and outs of the striatum: Role in drug addiction". Neuroscience. ج. 301: 529–541. DOI:10.1016/j.neuroscience.2015.06.033. PMC:4523218. PMID:26116518. [The striatum] receives dopaminergic inputs from the ventral tegmental area (VTA) and the substantia nigra (SNr) and glutamatergic inputs from several areas, including the cortex, hippocampus, amygdala, and thalamus (Swanson, 1982; Phillipson and Griffiths, 1985; Finch, 1996; Groenewegen et al., 1999; Britt et al., 2012). These glutamatergic inputs make contact on the heads of dendritic spines of the striatal GABAergic medium spiny projection neurons (MSNs) whereas dopaminergic inputs synapse onto the spine neck, allowing for an important and complex interaction between these two inputs in modulation of MSN activity ... It should also be noted that there is a small population of neurons in the [nucleus accumbens] NAc that coexpress both D1 and D2 receptors, though this is largely restricted to the NAc shell (Bertran- Gonzalez et al., 2008). ... Neurons in the NAc core and NAc shell subdivisions also differ functionally. The NAc core is involved in the processing of conditioned stimuli whereas the NAc shell is more important in the processing of unconditioned stimuli; Classically, these two striatal MSN populations are thought to have opposing effects on basal ganglia output. Activation of the dMSNs causes a net excitation of the thalamus resulting in a positive cortical feedback loop; thereby acting as a 'go' signal to initiate behavior. Activation of the iMSNs, however, causes a net inhibition of thalamic activity resulting in a negative cortical feedback loop and therefore serves as a 'brake' to inhibit behavior ... there is also mounting evidence that iMSNs play a role in motivation and addiction (Lobo and Nestler, 2011; Grueter et al., 2013). For example, optogenetic activation of NAc core and shell iMSNs suppressed the development of a cocaine CPP whereas selective ablation of NAc core and shell iMSNs ... enhanced the development and the persistence of an amphetamine CPP (Durieux et al., 2009; Lobo et al., 2010). These findings suggest that iMSNs can bidirectionally modulate drug reward. ... Together these data suggest that iMSNs normally act to restrain drug-taking behavior and recruitment of these neurons may in fact be protective against the development of compulsive drug use.
↑  Taylor SB، Lewis CR، Olive MF (2013). "The neurocircuitry of illicit psychostimulant addiction: acute and chronic effects in humans". Subst Abuse Rehabil. ج. 4: 29–43. DOI:10.2147/SAR.S39684. PMC:3931688. PMID:24648786. Regions of the basal ganglia, which include the dorsal and ventral striatum, internal and external segments of the globus pallidus, subthalamic nucleus, and dopaminergic cell bodies in the substantia nigra, are highly implicated not only in fine motor control but also in [prefrontal cortex] PFC function.43 Of these regions, the [nucleus accumbens] NAc (described above) and the [dorsal striatum] DS (described below) are most frequently examined with respect to addiction. Thus, only a brief description of the modulatory role of the basal ganglia in addiction-relevant circuits will be mentioned here. The overall output of the basal ganglia is predominantly via the thalamus, which then projects back to the PFC to form cortico-striatal-thalamo-cortical (CSTC) loops. Three CSTC loops are proposed to modulate executive function, action selection, and behavioral inhibition. In the dorsolateral prefrontal circuit, the basal ganglia primarily modulate the identification and selection of goals, including rewards.44 The [orbitofrontal cortex] OFC circuit modulates decision-making and impulsivity, and the anterior cingulate circuit modulates the assessment of consequences.44 These circuits are modulated by dopaminergic inputs from the [ventral tegmental area] VTA to ultimately guide behaviors relevant to addiction, including the persistence and narrowing of the behavioral repertoire toward drug seeking, and continued drug use despite negative consequences.43–45{{استشهاد بدورية محكمة}}:  صيانة الاستشهاد: دوي مجاني غير معلم (link)
↑  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. ج. 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.
1 2  Malenka RC, Nestler EJ, Hyman SE (2009). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (ط. 2nd). New York: McGraw-Hill Medical. ص. 365–366, 376. ISBN:978-0-07-148127-4. 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.{{استشهاد بكتاب}}:  صيانة الاستشهاد: أسماء متعددة: قائمة المؤلفين (link)
↑  Luo M، Zhou J، Liu Z (أغسطس 2015). "Reward processing by the dorsal raphe nucleus: 5-HT and beyond". Learn. Mem. ج. 22 ع. 9: 452–460. DOI:10.1101/lm.037317.114. PMC:4561406. PMID:26286655.
↑  Moulton EA، Elman I، Becerra LR، Goldstein RZ، Borsook D (مايو 2014). "The cerebellum and addiction: insights gained from neuroimaging research". Addict. Biol. ج. 19 ع. 3: 317–331. DOI:10.1111/adb.12101. PMC:4031616. PMID:24851284.
↑  Caligiore D، Pezzulo G، Baldassarre G، Bostan AC، Strick PL، Doya K، Helmich RC، Dirkx M، Houk J، Jörntell H، Lago-Rodriguez A، Galea JM، Miall RC، Popa T، Kishore A، Verschure PF، Zucca R، Herreros I (فبراير 2017). "Consensus Paper: Towards a Systems-Level View of Cerebellar Function: the Interplay Between Cerebellum, Basal Ganglia, and Cortex". Cerebellum. ج. 16 ع. 1: 203–229. DOI:10.1007/s12311-016-0763-3. PMC:5243918. PMID:26873754.
↑  
Carlson, Neil R. Physiology of Behavior. 11th ed. Boston: Pearson, 2013. Print.
↑  Wise RA، Rompre PP (1989). "Brain dopamine and reward". Annual Review of Psychology. ج. 40: 191–225. DOI:10.1146/annurev.ps.40.020189.001203. PMID:2648975.
↑  Wise RA (أكتوبر 2002). "Brain reward circuitry: insights from unsensed incentives". Neuron. ج. 36 ع. 2: 229–240. DOI:10.1016/S0896-6273(02)00965-0. PMID:12383779.
↑  Nucleus Accumbens نسخة محفوظة 2 أكتوبر 2020 على موقع واي باك مشين.
↑  Trantham-Davidson H، Neely LC، Lavin A، Seamans JK (2004). "Mechanisms underlying differential D1 versus D2 dopamine receptor regulation of inhibition in prefrontal cortex". The Journal of Neuroscience. ج. 24 ع. 47: 10652–10659. DOI:10.1523/jneurosci.3179-04.2004. PMID:15564581.
↑  You ZB، Chen YQ، Wise RA (2001). "Dopamine and glutamate release in the nucleus accumbens and ventral tegmental area of rat following lateral hypothalamic self-stimulation". Neuroscience. ج. 107 ع. 4: 629–639. DOI:10.1016/s0306-4522(01)00379-7. PMID:11720786.
↑  Kolb B, Whishaw IQ (2001). An Introduction to Brain and Behavior (ط. 1st). New York: Worth. ص. 438–441. ISBN:9780716751694. مؤرشف من الأصل في 2019-12-17.
↑  Richard JM، Castro DC، Difeliceantonio AG، Robinson MJ، Berridge KC (نوفمبر 2013). "Mapping brain circuits of reward and motivation: in the footsteps of Ann Kelley". Neurosci. Biobehav. Rev. ج. 37 ع. 9 Pt A: 1919–1931. DOI:10.1016/j.neubiorev.2012.12.008. PMC:3706488. PMID:23261404. 
Figure 3: Neural circuits underlying motivated 'wanting' and hedonic 'liking'. {{استشهاد بدورية محكمة}}: روابط خارجية في |اقتباس= (مساعدة)
1 2  Berridge KC، Kringelbach ML (1 يونيو 2013). "Neuroscience of affect: brain mechanisms of pleasure and displeasure". Current Opinion in Neurobiology. ج. 23 ع. 3: 294–303. DOI:10.1016/j.conb.2013.01.017. PMC:3644539. PMID:23375169. For instance, mesolimbic dopamine, probably the most popular brain neurotransmitter candidate for pleasure two decades ago, turns out not to cause pleasure or liking at all. Rather dopamine more selectively mediates a motivational process of incentive salience, which is a mechanism for wanting rewards but not for liking them .... Rather opioid stimulation has the special capacity to enhance liking only if the stimulation occurs within an anatomical hotspot
↑  Kringelbach ML, Berridge KC (2012). "The Joyful Mind". Scientific American: 44–45. مؤرشف من الأصل (PDF) في 2019-06-17. اطلع عليه بتاريخ 2017-01-17. So it makes sense that the real pleasure centers in the brain – those directly responsible for generating pleasurable sensations – turn out to lie within some of the structures previously identified as part of the reward circuit. One of these so-called hedonic hotspots lies in a subregion of the nucleus accumbens called the medial shell. A second is found within the ventral pallidum, a deep-seated structure near the base of the forebrain that receives most of its signals from the nucleus accumbens. ... 
     On the other hand, intense euphoria is harder to come by than everyday pleasures.  The reason may be that strong enhancement of pleasure – like the chemically induced pleasure bump we produced in lab animals – seems to require activation of the entire network at once. Defection of any single component dampens the high.
     Whether the pleasure circuit – and in particular, the ventral pallidum – works the same way in humans is unclear.
↑  Berridge KC (أبريل 2012). "From prediction error to incentive salience: mesolimbic computation of reward motivation". Eur. J. Neurosci. ج. 35 ع. 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.
Cue-triggered 'wanting' for the UCS
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.
Cue as attractive motivational magnets
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 ... 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.
↑  Malenka RC, Nestler EJ, Hyman SE (2009). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (ط. 2nd). New York: McGraw-Hill Medical. ص. 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.{{استشهاد بكتاب}}:  صيانة الاستشهاد: أسماء متعددة: قائمة المؤلفين (link)
↑  Salamone JD، Correa M (8 نوفمبر 2012). "The mysterious motivational functions of mesolimbic dopamine". Neuron. ج. 76 ع. 3: 470–485. DOI:10.1016/j.neuron.2012.10.021. ISSN:1097-4199. PMC:4450094. PMID:23141060.
1 2  Calipari ES، Bagot RC، Purushothaman I، Davidson TJ، Yorgason JT، Peña CJ، Walker DM، Pirpinias ST، Guise KG، Ramakrishnan C، Deisseroth K، Nestler EJ (مارس 2016). "In vivo imaging identifies temporal signature of D1 and D2 medium spiny neurons in cocaine reward". Proc. Natl. Acad. Sci. U.S.A. ج. 113 ع. 10: 2726–2731. DOI:10.1073/pnas.1521238113. PMC:4791010. PMID:26831103. Previous work has demonstrated that optogenetically stimulating D1 [medium spiny neurons] MSNs promotes reward, whereas stimulating D2 MSNs produces aversion. ... Studies using in vivo pharmacological approaches have demonstrated differential roles of NAc D1 and D2 receptors in drug conditioning by use of selective receptor agonists or antagonists, further supporting a role for both dopamine and D1 and D2 MSN subtypes in associative learning (27). Whereas this work has focused on the VTA-to-NAc dopamine circuit, tracking postsynaptic responses in NAc MSNs is particularly important because they integrate information not only from VTA dopamine neurons but also from numerous glutamatergic projections (28, 29). From a network perspective, D1 and D2 MSNs receive inputs from several regions known to encode and store information about context or context–drug associations such as the prefrontal cortex, basolateral amygdala, and hippocampus (30). ... Our data highlight the important role played by D1 MSNs in NAc core in establishing context–reward associations and in controlling the strength of these associations after cocaine exposure. ... Here we show that regulation of associative learning, and its dysregulation by cocaine, is driven primarily through alterations in D1 MSNs in NAc core, which both impair the extinction of previously learned associations and enhance reinstatement following abstinence.
1 2  Baliki MN، Mansour A، Baria AT، Huang L، Berger SE، Fields HL، Apkarian AV (أكتوبر 2013). "Parceling human accumbens into putative core and shell dissociates encoding of values for reward and pain". J. Neurosci. ج. 33 ع. 41: 16383–16393. DOI:10.1523/JNEUROSCI.1731-13.2013. PMC:3792469. PMID:24107968. Recent evidence indicates that inactivation of D2 receptors, in the indirect striatopallidal pathway in rodents, is necessary for both acquisition and expression of aversive behavior, and direct pathway D1 receptor activation controls reward-based learning (Hikida et al., 2010; Hikida et al., 2013). It seems we can conclude that direct and indirect pathways of the NAc, via D1 and D2 receptors, subserve distinct anticipation and valuation roles in the shell and core of NAc, which is consistent with observations regarding spatial segregation and diversity of responses of midbrain dopaminergic neurons for rewarding and aversive conditions, some encoding motivational value, others motivational salience, each connected with distinct brain networks and having distinct roles in motivational control (Bromberg-Martin et al., 2010; Cohen et al., 2012; Lammel et al., 2013). ... Thus, the previous results, coupled with the current observations, imply that the NAc pshell response reflects a prediction/anticipation or salience signal, and the NAc pcore response is a valuation response (reward predictive signal) that signals the negative reinforcement value of cessation of pain (i.e., anticipated analgesia).