References analysis of the Wikipedia article "報酬系" in the Japanese version

doi.org

“Neuronal reward and decision signals: from theories to data”. Physiological Reviews 95 (3): 853–951. (2015). 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, sexual 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. 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. 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. 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 and strongly support the learning and approach generating functions of reward."

“Neurobiologic Advances from the Brain Disease Model of Addiction”. N. Engl. J. Med. 374 (4): 363–371. (January 2016). doi:10.1056/NEJMra1511480. PMID 26816013.

Schultz, Wolfram (July 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.

“Pleasure systems in the brain”. Neuron 86 (3): 646–664. (May 2015). 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)."

Guo, Rong; Böhmer, Wendelin; Hebart, Martin; Chien, Samson; Sommer, Tobias; Obermayer, Klaus; Gläscher, Jan (2016-12-14). “Interaction of Instrumental and Goal-Directed Learning Modulates Prediction Error Representations in the Ventral Striatum”. The Journal of Neuroscience (Society for Neuroscience) 36 (50): 12650–12660. doi:10.1523/jneurosci.1677-16.2016. ISSN 0270-6474. PMC 6705659. PMID 27974615.

Duarte, Isabel C.; Afonso, Sónia; Jorge, Helena; Cayolla, Ricardo; Ferreira, Carlos; Castelo-Branco, Miguel (1 May 2017). “Tribal love: the neural correlates of passionate engagement in football fans”. Social Cognitive and Affective Neuroscience 12 (5): 718–728. doi:10.1093/scan/nsx003. PMC 5460049. PMID 28338882.

Salamone, John D.; Correa, Mercè (November 2012). “The Mysterious Motivational Functions of Mesolimbic Dopamine”. Neuron 76 (3): 470–485. doi:10.1016/j.neuron.2012.10.021. PMC 4450094. PMID 23141060.

“The ins and outs of the striatum: Role in drug addiction”. Neuroscience 301: 529–541. (August 2015). 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."

“The neurocircuitry of illicit psychostimulant addiction: acute and chronic effects in humans”. Subst Abuse Rehabil 4: 29–43. (2013). 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"

“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. (2014). 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."

“Mapping brain circuits of reward and motivation: in the footsteps of Ann Kelley”. Neurosci. Biobehav. Rev. 37 (9 Pt A): 1919–1931. (November 2013). doi:10.1016/j.neubiorev.2012.12.008. PMC 3706488. PMID 23261404.
Figure 3: Neural circuits underlying motivated 'wanting' and hedonic 'liking'.

“Reward processing by the dorsal raphe nucleus: 5-HT and beyond”. Learn. Mem. 22 (9): 452–460. (August 2015). doi:10.1101/lm.037317.114. PMC 4561406. PMID 26286655.

“The cerebellum and addiction: insights gained from neuroimaging research”. Addiction Biology 19 (3): 317–331. (May 2014). doi:10.1111/adb.12101. PMC 4031616. PMID 24851284.

“Consensus Paper: Towards a Systems-Level View of Cerebellar Function: the Interplay Between Cerebellum, Basal Ganglia, and Cortex”. Cerebellum 16 (1): 203–229. (February 2017). doi:10.1007/s12311-016-0763-3. PMC 5243918. PMID 26873754.

Ogawa, SK; Watabe-Uchida, M (2018). “Organization of dopamine and serotonin system: Anatomical and functional mapping of monosynaptic inputs using rabies virus”. Pharmacology Biochemistry and Behavior 174: 9–22. doi:10.1016/j.pbb.2017.05.001. PMID 28476484.

Morales, M; Margolis, EB (February 2017). “Ventral tegmental area: cellular heterogeneity, connectivity and behaviour”. Nature Reviews. Neuroscience 18 (2): 73–85. doi:10.1038/nrn.2016.165. PMID 28053327.

Lammel, S; Lim, BK; Malenka, RC (January 2014). “Reward and aversion in a heterogeneous midbrain dopamine system”. Neuropharmacology 76 Pt B: 351–9. doi:10.1016/j.neuropharm.2013.03.019. PMC 3778102. PMID 23578393.

Nieh, EH; Kim, SY; Namburi, P; Tye, KM (20 May 2013). “Optogenetic dissection of neural circuits underlying emotional valence and motivated behaviors”. Brain Research 1511: 73–92. doi:10.1016/j.brainres.2012.11.001. hdl:1721.1/92890. PMC 4099056. PMID 23142759.

“Mechanisms underlying differential D1 versus D2 dopamine receptor regulation of inhibition in prefrontal cortex”. The Journal of Neuroscience 24 (47): 10652–10659. (2004). doi:10.1523/jneurosci.3179-04.2004. PMC 5509068. PMID 15564581.

“Dopamine and glutamate release in the nucleus accumbens and ventral tegmental area of rat following lateral hypothalamic self-stimulation”. Neuroscience 107 (4): 629–639. (2001). doi:10.1016/s0306-4522(01)00379-7. PMID 11720786.

Castro, DC; Cole, SL; Berridge, KC (2015). “Lateral hypothalamus, nucleus accumbens, and ventral pallidum roles in eating and hunger: interactions between homeostatic and reward circuitry”. Frontiers in Systems Neuroscience 9: 90. doi:10.3389/fnsys.2015.00090. PMC 4466441. PMID 26124708.

Carlezon WA, Jr; Thomas, MJ (2009). “Biological substrates of reward and aversion: a nucleus accumbens activity hypothesis”. Neuropharmacology 56 (Suppl 1): 122–32. doi:10.1016/j.neuropharm.2008.06.075. PMC 2635333. PMID 18675281.

“Brain dopamine and reward”. Annual Review of Psychology 40: 191–225. (1989). doi:10.1146/annurev.ps.40.020189.001203. PMID 2648975.

“Brain reward circuitry: insights from unsensed incentives”. Neuron 36 (2): 229–240. (October 2002). doi:10.1016/S0896-6273(02)00965-0. PMID 12383779.

Chau, Bolton (2018). “Dopamine and reward: a view from the prefrontal cortex”. Behavioural Pharmacology 29 (7): 569–583. doi:10.1097/FBP.0000000000000424. PMID 30188354.

Castro, DC; Berridge, KC (24 October 2017). “Opioid and orexin hedonic hotspots in rat orbitofrontal cortex and insula”. Proceedings of the National Academy of Sciences of the United States of America 114 (43): E9125–E9134. Bibcode: 2017PNAS..114E9125C. doi:10.1073/pnas.1705753114. PMC 5664503. PMID 29073109. "Here, we show that opioid or orexin stimulations in orbitofrontal cortex and insula causally enhance hedonic "liking" reactions to sweetness and find a third cortical site where the same neurochemical stimulations reduce positive hedonic impact."

“An Update on the Role of Serotonin and its Interplay with Dopamine for Reward”. Front Hum Neurosci 11: 484. (2017). doi:10.3389/fnhum.2017.00484. PMC 5641585. PMID 29075184. "It has long been known from animal studies across different species that the raphe nuclei, the origin of most of the forebrain's serotonergic innervation, are among the most potent areas inducing self stimulation equivalent to stimulation of the medial forebrain bundle or the ventral tegmental area (VTA; Miliaressis et al., 1975; Van Der Kooy et al., 1978; Rompre and Miliaressis, 1985)."

“The Joyful Mind”. Scientific American 307 (2): 44–45. (2012). Bibcode: 2012SciAm.307b..40K. doi:10.1038/scientificamerican0812-40. PMID 22844850. オリジナルの29 March 2017時点におけるアーカイブ。 2017年1月17日閲覧. "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."

“From prediction error to incentive salience: mesolimbic computation of reward motivation”. Eur. J. Neurosci. 35 (7): 1124–1143. (April 2012). 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."

“Neuroscience of affect: brain mechanisms of pleasure and displeasure”. Current Opinion in Neurobiology 23 (3): 294–303. (1 June 2013). 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"

Calipari, Erin S.; Bagot, Rosemary C.; Purushothaman, Immanuel; Davidson, Thomas J.; Yorgason, Jordan T.; Peña, Catherine J.; Walker, Deena M.; Pirpinias, Stephen T. et al. (8 March 2016). “In vivo imaging identifies temporal signature of D1 and D2 medium spiny neurons in cocaine reward”. Proceedings of the National Academy of Sciences 113 (10): 2726–2731. Bibcode: 2016PNAS..113.2726C. doi:10.1073/pnas.1521238113. PMC 4791010. PMID 26831103.

Baliki, M. N.; Mansour, A.; Baria, A. T.; Huang, L.; Berger, S. E.; Fields, H. L.; Apkarian, A. V. (9 October 2013). “Parceling Human Accumbens into Putative Core and Shell Dissociates Encoding of Values for Reward and Pain”. Journal of Neuroscience 33 (41): 16383–16393. doi:10.1523/JNEUROSCI.1731-13.2013. PMC 3792469. PMID 24107968.

Soares-Cunha, Carina; Coimbra, Barbara; Sousa, Nuno; Rodrigues, Ana J. (September 2016). “Reappraising striatal D1- and D2-neurons in reward and aversion”. Neuroscience & Biobehavioral Reviews 68: 370–386. doi:10.1016/j.neubiorev.2016.05.021. hdl:1822/47044. PMID 27235078.

Bamford, Nigel S.; Wightman, R. Mark; Sulzer, David (February 2018). “Dopamine's Effects on Corticostriatal Synapses during Reward-Based Behaviors”. Neuron 97 (3): 494–510. doi:10.1016/j.neuron.2018.01.006. PMC 5808590. PMID 29420932.

Soares-Cunha, Carina; Coimbra, Barbara; David-Pereira, Ana; Borges, Sonia; Pinto, Luisa; Costa, Patricio; Sousa, Nuno; Rodrigues, Ana J. (September 2016). “Activation of D2 dopamine receptor-expressing neurons in the nucleus accumbens increases motivation”. Nature Communications 7 (1): 11829. Bibcode: 2016NatCo...711829S. doi:10.1038/ncomms11829. PMC 4931006. PMID 27337658.

Soares-Cunha, Carina; Coimbra, Bárbara; Domingues, Ana Verónica; Vasconcelos, Nivaldo; Sousa, Nuno; Rodrigues, Ana João (March 2018). “Nucleus Accumbens Microcircuit Underlying D2-MSN-Driven Increase in Motivation”. eNeuro 5 (2): ENEURO.0386–18.2018. doi:10.1523/ENEURO.0386-18.2018. PMC 5957524. PMID 29780881.

Yin, HH; Ostlund, SB; Balleine, BW (October 2008). “Reward-guided learning beyond dopamine in the nucleus accumbens: the integrative functions of cortico-basal ganglia networks”. The European Journal of Neuroscience 28 (8): 1437–48. doi:10.1111/j.1460-9568.2008.06422.x. PMC 2756656. PMID 18793321.

Dayan, P; Berridge, KC (June 2014). “Model-based and model-free Pavlovian reward learning: revaluation, revision, and revelation”. Cognitive, Affective, & Behavioral Neuroscience 14 (2): 473–92. doi:10.3758/s13415-014-0277-8. PMC 4074442. PMID 24647659.

Balleine, BW; Morris, RW; Leung, BK (2 December 2015). “Thalamocortical integration of instrumental learning and performance and their disintegration in addiction”. Brain Research 1628 (Pt A): 104–16. doi:10.1016/j.brainres.2014.12.023. PMID 25514336. "Importantly, we found evidence of increased activity in the direct pathway; both intracellular changes in the expression of the plasticity marker pERK and AMPA/NMDA ratios evoked by stimulating cortical afferents were increased in the D1-direct pathway neurons. In contrast, D2 neurons showed an opposing change in plasticity; stimulation of cortical afferents reduced AMPA/NMDA ratios on those neurons (Shan et al., 2014)."

Nakanishi, S; Hikida, T; Yawata, S (12 December 2014). “Distinct dopaminergic control of the direct and indirect pathways in reward-based and avoidance learning behaviors”. Neuroscience 282: 49–59. doi:10.1016/j.neuroscience.2014.04.026. PMID 24769227.

Shiflett, MW; Balleine, BW (15 September 2011). “Molecular substrates of action control in cortico-striatal circuits”. Progress in Neurobiology 95 (1): 1–13. doi:10.1016/j.pneurobio.2011.05.007. PMC 3175490. PMID 21704115.

Schultz, W (April 2013). “Updating dopamine reward signals”. Current Opinion in Neurobiology 23 (2): 229–38. doi:10.1016/j.conb.2012.11.012. PMC 3866681. PMID 23267662.

Shiflett, MW; Balleine, BW (17 March 2011). “Contributions of ERK signaling in the striatum to instrumental learning and performance”. Behavioural Brain Research 218 (1): 240–7. doi:10.1016/j.bbr.2010.12.010. PMC 3022085. PMID 21147168.

Ruffle JK (November 2014). “Molecular neurobiology of addiction: what's all the (Δ)FosB about?”. Am. J. Drug Alcohol Abuse 40 (6): 428–437. doi:10.3109/00952990.2014.933840. PMID 25083822. "
The strong correlation between chronic drug exposure and ΔFosB provides novel opportunities for targeted therapies in addiction (118), and suggests methods to analyze their efficacy (119). Over the past two decades, research has progressed from identifying ΔFosB induction to investigating its subsequent action (38). It is likely that ΔFosB research will now progress into a new era – the use of ΔFosB as a biomarker. ...
Conclusions
ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. The formation of ΔFosB in multiple brain regions, and the molecular pathway leading to the formation of AP-1 complexes is well understood. The establishment of a functional purpose for ΔFosB has allowed further determination as to some of the key aspects of its molecular cascades, involving effectors such as GluR2 (87,88), Cdk5 (93) and NFkB (100). Moreover, many of these molecular changes identified are now directly linked to the structural, physiological and behavioral changes observed following chronic drug exposure (60,95,97,102). New frontiers of research investigating the molecular roles of ΔFosB have been opened by epigenetic studies, and recent advances have illustrated the role of ΔFosB acting on DNA and histones, truly as a molecular switch (34). As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction."

Olsen CM (December 2011). “Natural rewards, neuroplasticity, and non-drug addictions”. Neuropharmacology 61 (7): 1109–1122. doi:10.1016/j.neuropharm.2011.03.010. PMC 3139704. PMID 21459101. "Functional neuroimaging studies in humans have shown that gambling (Breiter et al, 2001), shopping (Knutson et al, 2007), orgasm (コミサルク（英語版） et al, 2004), playing video games (Koepp et al, 1998; Hoeft et al, 2008) and the sight of appetizing food (Wang et al, 2004a) activate many of the same brain regions (i.e., the mesocorticolimbic system and extended amygdala) as drugs of abuse (Volkow et al, 2004). ... Cross-sensitization is also bidirectional, as a history of amphetamine administration facilitates sexual behavior and enhances the associated increase in NAc DA ... As described for food reward, sexual experience can also lead to activation of plasticity-related signaling cascades. The transcription factor delta FosB is increased in the NAc, PFC, dorsal striatum, and VTA following repeated sexual behavior (Wallace et al., 2008; Pitchers et al., 2010b). This natural increase in delta FosB or viral overexpression of delta FosB within the NAc modulates sexual performance, and NAc blockade of delta FosB attenuates this behavior (Hedges et al, 2009; Pitchers et al., 2010b). Further, viral overexpression of delta FosB enhances the conditioned place preference for an environment paired with sexual experience (Hedges et al., 2009). ... In some people, there is a transition from "normal" to compulsive engagement in natural rewards (such as food or sex), a condition that some have termed behavioral or non-drug addictions (Holden, 2001; Grant et al., 2006a). ... In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients taking dopaminergic drugs. This syndrome is characterized by a medication-induced increase in (or compulsive) engagement in non-drug rewards such as gambling, shopping, or sex (Evans et al, 2006; Aiken, 2007; Lader, 2008).""
Table 1: Summary of plasticity observed following exposure to drug or natural reinforcers"

“Natural and drug rewards act on common neural plasticity mechanisms with ΔFosB as a key mediator”. The Journal of Neuroscience（英語版） 33 (8): 3434–3442. (February 2013). doi:10.1523/JNEUROSCI.4881-12.2013. PMC 3865508. PMID 23426671. "Drugs of abuse induce neuroplasticity in the natural reward pathway, specifically the nucleus accumbens (NAc), thereby causing development and expression of addictive behavior. ... Together, these findings demonstrate that drugs of abuse and natural reward behaviors act on common molecular and cellular mechanisms of plasticity that control vulnerability to drug addiction, and that this increased vulnerability is mediated by ΔFosB and its downstream transcriptional targets. ... Sexual behavior is highly rewarding (Tenk et al., 2009), and sexual experience causes sensitized drug-related behaviors, including cross-sensitization to amphetamine (Amph)-induced locomotor activity (Bradley and Meisel, 2001; Pitchers et al., 2010a) and enhanced Amph reward (Pitchers et al., 2010a). Moreover, sexual experience induces neural plasticity in the NAc similar to that induced by psychostimulant exposure, including increased dendritic spine density (Meisel and Mullins, 2006; Pitchers et al., 2010a), altered glutamate receptor trafficking, and decreased synaptic strength in prefrontal cortex-responding NAc shell neurons (Pitchers et al., 2012). Finally, periods of abstinence from sexual experience were found to be critical for enhanced Amph reward, NAc spinogenesis (Pitchers et al., 2010a), and glutamate receptor trafficking (Pitchers et al., 2012). These findings suggest that natural and drug reward experiences share common mechanisms of neural plasticity"

“Nucleus accumbens NMDA receptor activation regulates amphetamine cross-sensitization and deltaFosB expression following sexual experience in male rats”. Neuropharmacology 101: 154–164. (February 2016). doi:10.1016/j.neuropharm.2015.09.023. PMID 26391065.

“Transcriptional and epigenetic mechanisms of addiction”. Nat. Rev. Neurosci. 12 (11): 623–637. (November 2011). doi:10.1038/nrn3111. PMC 3272277. PMID 21989194. "ΔFosB serves as one of the master control proteins governing this structural plasticity. ... ΔFosB also represses G9a expression, leading to reduced repressive histone methylation at the cdk5 gene. The net result is gene activation and increased CDK5 expression. ... In contrast, ΔFosB binds to the c-fos gene and recruits several co-repressors, including HDAC1 (histone deacetylase 1) and SIRT 1 (sirtuin 1). ... The net result is c-fos gene repression."
Figure 4: Epigenetic basis of drug regulation of gene expression

“Histone-mediated epigenetics in addiction”. Epigenetics and Neuroplasticity—Evidence and Debate. Progress in Molecular Biology and Translational Science. 128. (2014). 51–87. doi:10.1016/B978-0-12-800977-2.00003-6. ISBN 9780128009772. PMC 5914502. PMID 25410541

“Neuroepigenetics and addiction”. Neurogenetics, Part II. Handbook of Clinical Neurology. 148. (2018). pp. 747–765. doi:10.1016/B978-0-444-64076-5.00048-X. ISBN 9780444640765. PMC 5868351. PMID 29478612

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Rømer Thomsen, K; Whybrow, PC; Kringelbach, ML (2015). “Reconceptualizing anhedonia: novel perspectives on balancing the pleasure networks in the human brain”. Frontiers in Behavioral Neuroscience 9: 49. doi:10.3389/fnbeh.2015.00049. PMC 4356228. PMID 25814941.

Thomsen, KR (2015). “Measuring anhedonia: impaired ability to pursue, experience, and learn about reward”. Frontiers in Psychology 6: 1409. doi:10.3389/fpsyg.2015.01409. PMC 4585007. PMID 26441781.

Olney, JJ; Warlow, SM; Naffziger, EE; Berridge, KC (August 2018). “Current perspectives on incentive salience and applications to clinical disorders”. Current Opinion in Behavioral Sciences 22: 59–69. doi:10.1016/j.cobeha.2018.01.007. PMC 5831552. PMID 29503841.

Zhang, B; Lin, P; Shi, H; Öngür, D; Auerbach, RP; Wang, X; Yao, S; Wang, X (September 2016). “Mapping anhedonia-specific dysfunction in a transdiagnostic approach: an ALE meta-analysis”. Brain Imaging and Behavior 10 (3): 920–39. doi:10.1007/s11682-015-9457-6. PMC 4838562. PMID 26487590.

Salamone, JD; Yohn, SE; López-Cruz, L; San Miguel, N; Correa, M (May 2016). “Activational and effort-related aspects of motivation: neural mechanisms and implications for psychopathology”. Brain: A Journal of Neurology 139 (Pt 5): 1325–47. doi:10.1093/brain/aww050. PMC 5839596. PMID 27189581.

Russo, SJ; Nestler, EJ (September 2013). “The brain reward circuitry in mood disorders”. Nature Reviews. Neuroscience 14 (9): 609–25. doi:10.1038/nrn3381. PMC 3867253. PMID 23942470.

Treadway, MT; Zald, DH (January 2011). “Reconsidering anhedonia in depression: lessons from translational neuroscience”. Neuroscience and Biobehavioral Reviews 35 (3): 537–55. doi:10.1016/j.neubiorev.2010.06.006. PMC 3005986. PMID 20603146.

Walsh, JJ; Han, MH (12 December 2014). “The heterogeneity of ventral tegmental area neurons: Projection functions in a mood-related context”. Neuroscience 282: 101–8. doi:10.1016/j.neuroscience.2014.06.006. PMC 4339667. PMID 24931766.

Knowland, D; Lim, BK (5 January 2018). “Circuit-based frameworks of depressive behaviors: The role of reward circuitry and beyond”. Pharmacology Biochemistry and Behavior 174: 42–52. doi:10.1016/j.pbb.2017.12.010. PMC 6340396. PMID 29309799.

Lammel, S; Tye, KM; Warden, MR (January 2014). “Progress in understanding mood disorders: optogenetic dissection of neural circuits”. Genes, Brain and Behavior 13 (1): 38–51. doi:10.1111/gbb.12049. PMID 23682971.

Bucci, P; Galderisi, S (May 2017). “Categorizing and assessing negative symptoms”. Current Opinion in Psychiatry 30 (3): 201–208. doi:10.1097/YCO.0000000000000322. PMID 28212174. "They also provide a separate assessment of the consummatory anhedonia (reduced experience of pleasure derived from ongoing enjoyable activities) and anticipatory anhedonia (reduced ability to anticipate future pleasure). In fact, the former one seems to be relatively intact in schizophrenia, whereas the latter one seems to be impaired [32 – 34]. However, discrepant data have also been reported [35]."

“New perspectives on catecholaminergic regulation of executive circuits: evidence for independent modulation of prefrontal functions by midbrain dopaminergic and noradrenergic neurons”. Frontiers in Neural Circuits 8: 53. (May 2014). doi:10.3389/fncir.2014.00053. PMC 4033238. PMID 24904299.

Blum, Kenneth; Chen, Amanda Lih-Chuan; Braverman, Eric R; Comings, David E; Chen, Thomas JH; Arcuri, Vanessa; Blum, Seth H; Downs, Bernard W et al. (October 2008). “Attention-deficit-hyperactivity disorder and reward deficiency syndrome”. Neuropsychiatric Disease and Treatment 4 (5): 893–918. doi:10.2147/ndt.s2627. ISSN 1176-6328. PMC 2626918. PMID 19183781.

“Addictive drugs and brain stimulation reward”. Annu. Rev. Neurosci. 19: 319–340. (1996). doi:10.1146/annurev.ne.19.030196.001535. PMID 8833446.

James Olds and Peter Milner (Dec 1954). “Positive reinforcement produced by electrical stimulation of the septal area and other regions of rat brain”. Journal of Comparative and Physiological Psychology（英語版） 47 (6): 419–427. doi:10.1037/h0058775. PMID 13233369. オリジナルの5 February 2012時点におけるアーカイブ。 2011年4月26日閲覧。.

Han W, Tellez LA, Perkins MH, Perez IO, Qu T, Ferreira J (2018). “A Neural Circuit for Gut-Induced Reward.”. Cell 175 (3): 665–678.e23. doi:10.1016/j.cell.2018.08.049. PMC 6195474. PMID 30245012.

Berridge, Kent C.; Kringelbach, Morten L. (August 2008). “Affective neuroscience of pleasure: reward in humans and animals”. Psychopharmacology 199 (3): 457–480. doi:10.1007/s00213-008-1099-6. PMC 3004012. PMID 18311558.

“Dopamine modulates the reward experiences elicited by music”. Proceedings of the National Academy of Sciences of the United States of America 116 (9): 3793–3798. (January 2019). Bibcode: 2019PNAS..116.3793F. doi:10.1073/pnas.1811878116. PMC 6397525. PMID 30670642. "Listening to pleasurable music is often accompanied by measurable bodily reactions such as goose bumps or shivers down the spine, commonly called 'chills' or 'frissons.' ... Overall, our results straightforwardly revealed that pharmacological interventions bidirectionally modulated the reward responses elicited by music. In particular, we found that risperidone impaired participants' ability to experience musical pleasure, whereas levodopa enhanced it. ... Here, in contrast, studying responses to abstract rewards in human subjects, we show that manipulation of dopaminergic transmission affects both the pleasure (i.e., amount of time reporting chills and emotional arousal measured by EDA) and the motivational components of musical reward (money willing to spend). These findings suggest that dopaminergic signaling is a sine qua non condition not only for motivational responses, as has been shown with primary and secondary rewards, but also for hedonic reactions to music. This result supports recent findings showing that dopamine also mediates the perceived pleasantness attained by other types of abstract rewards and challenges previous findings in animal models on primary rewards, such as food."

“Musical pleasure and musical emotions”. Proceedings of the National Academy of Sciences of the United States of America 116 (9): 3364–3366. (February 2019). Bibcode: 2019PNAS..116.3364G. doi:10.1073/pnas.1900369116. PMC 6397567. PMID 30770455. "In a pharmacological study published in PNAS, Ferreri et al. (1) present evidence that enhancing or inhibiting dopamine signaling using levodopa or risperidone modulates the pleasure experienced while listening to music. ... In a final salvo to establish not only the correlational but also the causal implication of dopamine in musical pleasure, the authors have turned to directly manipulating dopaminergic signaling in the striatum, first by applying excitatory and inhibitory transcranial magnetic stimulation over their participants' left dorsolateral prefrontal cortex, a region known to modulate striatal function (5), and finally, in the current study, by administrating pharmaceutical agents able to alter dopamine synaptic availability (1), both of which influenced perceived pleasure, physiological measures of arousal, and the monetary value assigned to music in the predicted direction. ... While the question of the musical expression of emotion has a long history of investigation, including in PNAS (6), and the 1990s psychophysiological strand of research had already established that musical pleasure could activate the autonomic nervous system (7), the authors' demonstration of the implication of the reward system in musical emotions was taken as inaugural proof that these were veridical emotions whose study has full legitimacy to inform the neurobiology of our everyday cognitive, social, and affective functions (8). Incidentally, this line of work, culminating in the article by Ferreri et al. (1), has plausibly done more to attract research funding for the field of music sciences than any other in this community. The evidence of Ferreri et al. (1) provides the latest support for a compelling neurobiological model in which musical pleasure arises from the interaction of ancient reward/valuation systems (striatal–limbic–paralimbic) with more phylogenetically advanced perception/predictions systems (temporofrontal)."

harvard.edu

ui.adsabs.harvard.edu

nih.gov

pubmed.ncbi.nlm.nih.gov

Nestler EJ (December 2013). “Cellular basis of memory for addiction”. Dialogues Clin. Neurosci. 15 (4): 431–443. PMC 3898681. PMID 24459410. 引用エラー: 無効な <ref> タグ; name "Cellular basis"が異なる内容で複数回定義されています

“Neurobiologic Advances from the Brain Disease Model of Addiction”. N. Engl. J. Med. 374 (4): 363–371. (January 2016). doi:10.1056/NEJMra1511480. PMID 26816013.

Schultz, Wolfram (July 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.

“Reward processing by the dorsal raphe nucleus: 5-HT and beyond”. Learn. Mem. 22 (9): 452–460. (August 2015). doi:10.1101/lm.037317.114. PMC 4561406. PMID 26286655.

“The cerebellum and addiction: insights gained from neuroimaging research”. Addiction Biology 19 (3): 317–331. (May 2014). doi:10.1111/adb.12101. PMC 4031616. PMID 24851284.

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Chau, Bolton (2018). “Dopamine and reward: a view from the prefrontal cortex”. Behavioural Pharmacology 29 (7): 569–583. doi:10.1097/FBP.0000000000000424. PMID 30188354.

Schultz, W (April 2013). “Updating dopamine reward signals”. Current Opinion in Neurobiology 23 (2): 229–38. doi:10.1016/j.conb.2012.11.012. PMC 3866681. PMID 23267662.

“Epigenetic regulation in drug addiction”. Ann. Agric. Environ. Med. 19 (3): 491–496. (2012). PMID 23020045. "For these reasons, ΔFosB is considered a primary and causative transcription factor in creating new neural connections in the reward centre, prefrontal cortex, and other regions of the limbic system. This is reflected in the increased, stable and long-lasting level of sensitivity to cocaine and other drugs, and tendency to relapse even after long periods of abstinence. These newly constructed networks function very efficiently via new pathways as soon as drugs of abuse are further taken ... In this way, the induction of CDK5 gene expression occurs together with suppression of the G9A gene coding for dimethyltransferase acting on the histone H3. A feedback mechanism can be observed in the regulation of these 2 crucial factors that determine the adaptive epigenetic response to cocaine. This depends on ΔFosB inhibiting G9a gene expression, i.e. H3K9me2 synthesis which in turn inhibits transcription factors for ΔFosB. For this reason, the observed hyper-expression of G9a, which ensures high levels of the dimethylated form of histone H3, eliminates the neuronal structural and plasticity effects caused by cocaine by means of this feedback which blocks ΔFosB transcription"

Russo, SJ; Nestler, EJ (September 2013). “The brain reward circuitry in mood disorders”. Nature Reviews. Neuroscience 14 (9): 609–25. doi:10.1038/nrn3381. PMC 3867253. PMID 23942470.

“Addictive drugs and brain stimulation reward”. Annu. Rev. Neurosci. 19: 319–340. (1996). doi:10.1146/annurev.ne.19.030196.001535. PMID 8833446.

Kringelbach, Morten L.; Berridge, Kent C. (25 June 2010). “The Functional Neuroanatomy of Pleasure and Happiness”. Discovery Medicine 9 (49): 579–587. PMC 3008353. PMID 20587348.

pmc.ncbi.nlm.nih.gov

Schultz, Wolfram (July 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.

“Reward processing by the dorsal raphe nucleus: 5-HT and beyond”. Learn. Mem. 22 (9): 452–460. (August 2015). doi:10.1101/lm.037317.114. PMC 4561406. PMID 26286655.

“The cerebellum and addiction: insights gained from neuroimaging research”. Addiction Biology 19 (3): 317–331. (May 2014). doi:10.1111/adb.12101. PMC 4031616. PMID 24851284.

Schultz, W (April 2013). “Updating dopamine reward signals”. Current Opinion in Neurobiology 23 (2): 229–38. doi:10.1016/j.conb.2012.11.012. PMC 3866681. PMID 23267662.

Russo, SJ; Nestler, EJ (September 2013). “The brain reward circuitry in mood disorders”. Nature Reviews. Neuroscience 14 (9): 609–25. doi:10.1038/nrn3381. PMC 3867253. PMID 23942470.

Kringelbach, Morten L.; Berridge, Kent C. (25 June 2010). “The Functional Neuroanatomy of Pleasure and Happiness”. Discovery Medicine 9 (49): 579–587. PMC 3008353. PMID 20587348.

ncbi.nlm.nih.gov

Schultz, Wolfram (July 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.

“Reward processing by the dorsal raphe nucleus: 5-HT and beyond”. Learn. Mem. 22 (9): 452–460. (August 2015). doi:10.1101/lm.037317.114. PMC 4561406. PMID 26286655.

“The cerebellum and addiction: insights gained from neuroimaging research”. Addiction Biology 19 (3): 317–331. (May 2014). doi:10.1111/adb.12101. PMC 4031616. PMID 24851284.

Schultz, W (April 2013). “Updating dopamine reward signals”. Current Opinion in Neurobiology 23 (2): 229–38. doi:10.1016/j.conb.2012.11.012. PMC 3866681. PMID 23267662.

Russo, SJ; Nestler, EJ (September 2013). “The brain reward circuitry in mood disorders”. Nature Reviews. Neuroscience 14 (9): 609–25. doi:10.1038/nrn3381. PMC 3867253. PMID 23942470.

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