Talk:Reward system

From WikiProjectMed
Jump to navigation Jump to search

Refs to add

Music neuroscience

Reward system

Cognitive control (an only marginally related neuropsychology concept - storing these refs here for now)

Reflist

References

  1. ^ Kringelbach ML, Berridge KC (2013). "The Joyful Mind". From Abuse to Recovery: Understanding Addiction. Macmillan. pp. 199–207. ISBN 9781466842557. Retrieved 8 April 2016. 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.
  2. ^ Blum K, Simpatico T, Febo M, Rodriquez C, Dushaj K, Li M, Braverman ER, Demetrovics Z, Oscar-Berman M, Badgaiyan RD (May 2016). "Hypothesizing Music Intervention Enhances Brain Functional Connectivity Involving Dopaminergic Recruitment: Common Neuro-correlates to Abusable Drugs". Mol. Neurobiol. doi:10.1007/s12035-016-9934-y. PMID 27246565. The goal of this review is to explore the clinical significance of music listening on neuroplasticity and dopaminergic activation by understanding the role of music therapy in addictive behavior treatment. fMRI data has shown that music listening intensely modifies mesolimbic structural changes responsible for reward processing (e.g., nucleus accumbens [NAc]) and may control the emotional stimuli's effect on autonomic and physiological responses (e.g., hypothalamus). Music listening has been proven to induce the endorphinergic response blocked by naloxone, a common opioid antagonist.
  3. ^ Reybrouck M, Brattico E (March 2015). "Neuroplasticity beyond Sounds: Neural Adaptations Following Long-Term Musical Aesthetic Experiences". Brain Sci. 5 (1): 69–91. doi:10.3390/brainsci5010069. PMC 4390792. PMID 25807006. Moreover, early emotional reactions are often accompanied by involuntary motor tendencies, including bodily changes related to the response of the autonomic nervous system (mainly the sympathetic one) to the sound events and are in many cases, such as with basic emotions, constitutive of what identifies an emotion [93]. Among the most studied involuntary bodily reactions are the chills or frissons, namely shivers down the spine, or goose-bump skin, sometimes accompanied even by crying, in response to listening to very pleasurable, familiar music (see [94,95,96,97] for an overview). A behavioral and physiological study by Grewe et al. [98], however, did not find any difference in the frequency of the occurrence and nature of the chill responses in musicians as compared to non-musicians while they listened to pieces by Bach, Mozart and Puccini; on the other hand, familiarity with the music increased the frequency of chills. ... A recent study by Alluri et al. [161] further investigated the functional connectivity between the nucleus accumbens and the rest of the brain during music listening and how it is affected by musical expertise. The findings indicate that the left nucleus accumbens has increased connections with other regions of the limbic and paralimbic system in musicians, whereas the right nucleus accumbens becomes more coupled to the hippocampus in non-musicians and to the temporal pole and ventromedial frontal regions in musicians. These results confirm and extend the findings of increased connectivity comprising the nucleus accumbens and the frontal regions during rewarding music listening, obtained by [162]. These results are novel in showing that the connectivity of the regions controlling reward and pleasurable experience with regions related to motor control and cognitive processing increases with musical expertise. ... As such, we read the literature on music-derived neuroplasticity, structuring it on the basis of the subprocesses comprising a musical aesthetic experience. By doing this, we stressed the need for further research on important aspects of music playing and listening, such as proprioception, aesthetic evaluation and social interaction.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. ^ Mavridis IN (March 2015). "Music and the nucleus accumbens". Surg Radiol Anat. 37 (2): 121–125. doi:10.1007/s00276-014-1360-0. PMID 25102783. The functional connectivity between brain regions mediating reward, autonomic and cognitive processing provides insight into understanding why listening to music is one of the most rewarding and pleasurable human experiences. Musical stimuli can significantly increase extracellular DA levels in the NA. NA DA and serotonin were found significantly higher in animals exposed to music. Finally, passive listening to unfamiliar although liked music showed activations in the NA. ... Music can arouse feelings of euphoria and craving, similar to tangible rewards that involve the striatal DAergic system [16]. Reward value for music can be coded by activity levels in the NA, whose functional connectivity with auditory and frontal areas increases as a function of increasing musical reward [19]. ... Listening to pleasant music induces a strong response and significant activation of the VTA-mediated interaction of the NA with the hypothalamus, insula and orbitofrontal cortex [1].
    Conclusions
    Listening to music strongly modulates activity in a network of mesolimbic structures involved in reward processing including the NA. Music, acting as a positive pleasant emotion, increases NA DAergic activity. Specifically the NA is more involved during the experience of peak emotional responses to music. Reward value of music can be predicted by increased functional connectivity of auditory cortices, amygdala and ventromedial prefrontal regions with the NA. Further research is needed to improve our understanding of the NA role in the influence of music in our lives.
  5. ^ Zatorre RJ (March 2015). "Musical pleasure and reward: mechanisms and dysfunction". Ann. N. Y. Acad. Sci. 1337: 202–211. doi:10.1111/nyas.12677. PMID 25773636. Most people derive pleasure from music. Neuroimaging studies show that the reward system of the human brain is central to this experience. Specifically, the dorsal and ventral striatum release dopamine when listening to pleasurable music, and activity in these structures also codes the reward value of musical excerpts. Moreover, the striatum interacts with cortical mechanisms involved in perception and valuation of musical stimuli. ... Development of a questionnaire for music reward experiences has allowed the identification of separable factors associated with musical pleasure, described as music-seeking, emotion-evocation, mood regulation, sensorimotor, and social factors. Applying this questionnaire to a large sample uncovered approximately 5% of the population with low sensitivity to musical reward in the absence of generalized anhedonia or depression. Further study of this group revealed that there are individuals who respond normally both behaviorally and psychophysiologically to rewards other than music (e.g., monetary value) but do not experience pleasure from music despite normal music perception ability and preserved ability to identify intended emotions in musical passages.
  6. ^ Mansouri FA, Fehring DJ, Gaillard A, Jaberzadeh S, Parkington H (February 2016). "Sex dependency of inhibitory control functions". Biol. Sex Differ. 7: 11. doi:10.1186/s13293-016-0065-y. PMC 4746892. PMID 26862388.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  7. ^ Jiang J, Scolaro AJ, Bailey K, Chen A (June 2011). "The effect of music-induced mood on attentional networks". Int. J. Psychol. 46 (3): 214–222. doi:10.1080/00207594.2010.541255. PMID 22044234.

Seppi333 (Insert 2¢) 08:18, 17 August 2015 (UTC) Edited 21:36, 21 July 2016 (UTC)[reply]

Pleasure-Opioid revert

''rather opioid stimulation has the special capacity to enhance ‘liking’ only if the stimulation occurs within an anatomical hotspot whereas dopamine never does anywhere"

"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" — Preceding unsigned comment added by Petergstrom (talk • contribs) 17:20, 15 January 2017 (UTC)[reply]

Sigh. I'm willing to keep this in instead of reverting it again, but my issue with it is not the dopamine clause. It's the underlined word in the following sentence: "only opioid injections in the ventrorostral region of the nucleus accumbens is able to increase liking." A statement like "only opioids produce pleasure in the NAcc hotspot" isn't supported by the ref. The ref also states that endocannabinoids produce pleasure in hedonic hotspots. Seppi333 (Insert 2¢) 21:50, 15 January 2017 (UTC)[reply]
Without the "only", it's a correct statement which is supported, but I still don't think it actually gives a complete picture of what dopamine's role in pleasure is, since the NAcc neurons (i.e., the MSNs) where opioids bind to produce pleasure also express DA receptors (because they're MSNs). DA necessarily affects pleasure cognition because it signals through a hedonic hotspot, but how is still unclear. It doesn't appear to be associated with producing notable acute changes in hedonic liking at that hotspot though. Seppi333 (Insert 2¢) 21:50, 15 January 2017 (UTC)[reply]

Graphic rearrangement artifact

When the TOC is collapsed and one's browser is maximized there is a bizarre interaction between the lede graphic and the addiction and dependence glossary template. It does seem reasonable to place the template above the addiction section as being at the end of the article this would create a similar graphic artifact. Could the template be adjusted down slightly from its present placement to resolve the issue? — βox73 (৳alk) 01:44, 18 January 2017 (UTC)[reply]

Can you upload a screenshot? Also, let me know what browser you're using and your screen resolution so that I can try to replicate this. Seppi333 (Insert 2¢) 02:17, 18 January 2017 (UTC)[reply]
@Seppi333: Screeenshot. A similar thing happens at reinforcement because the template is placed just above the terminology section heading but easily fixed moving just below that heading. Thanks. — βox73 (৳alk) 03:40, 18 January 2017 (UTC)[reply]
How's it look now? Also, can you screenshot the glossary in the reinforcement article? It was intended to be displayed right alongside the TOC in that one. Seppi333 (Insert 2¢) 08:19, 18 January 2017 (UTC)[reply]
@Box73: I gather that this has fixed the issue on your screen? Also, I can't seem to reproduce any graphical abnormalities on my screen when using different zoom settings/browsers/devices in the reinforcement article. Can you be specific as to what you see on your display in that article? Seppi333 (Insert 2¢) 00:20, 21 January 2017 (UTC)[reply]

Recent content additions

@XUY49: Much of what was added to the addiction section was copy and pasted from the following source. I've quoted some of the material that was copied in this quote.

When some drugs of abuse are taken, they can release 2 to 10 times the amount of dopamine that natural rewards such as eating and sex do.15 In some cases, this occurs almost immediately... , and the effects can last much longer than those produced by natural rewards. The resulting effects on the brain’s pleasure circuit dwarf those produced by naturally rewarding behaviors ... The effect of such a powerful reward strongly motivates people to take drugs again and again
— https://www.drugabuse.gov/publications/drugs-brains-behavior-science-addiction/drugs-brain

  • This website does not satisfy Wikipedia's citation guideline for medical content: WP:MEDRS. This guideline is a lot stricter than the standard citation policy (WP:RS). You need to read this guideline if you intend to edit articles that cover medical (sub-)topics, otherwise you will likely end up seeing most of your edits which include medical claims reverted. The reason I've removed the material you've added to the addiction section is that it is medical content which is supported/cited by very outdated sources (see WP:MEDRS#Use up-to-date evidence) and/or this website (see WP:MEDRS#Choosing sources).
  • Also, I'd strongly suggest reading WP:COPYANDPASTE. This text happens to be in the public domain because it comes from a website which is hosted by the US government; however, if that had not been the case, copy/pasting that text into this article would constitute a copyright violation, which is a very serious issue (the policy on this topic is Wikipedia:Copyright violations).
  • Lastly, Wikipedia has a WP:MANUAL OF STYLE (aka "MOS") that covers how article content is supposed to be written and formatted. Most of the changes I made to the article following your original edit were done to either establish conformity with the MOS or mark sections that still needed minor revisions to establish conformity with the MOS.

If you have any questions about any of these policies or why I've made a particular edit to the article, just ask me. Wikipedia has a learning curve and I know that these guidelines/policies are fairly lengthy, so I'm willing to answer any questions you might have in order to help you become a better editor. Seppi333 (Insert 2¢) 09:15, 12 March 2017 (UTC)[reply]

D1/D2 MSN dichotomy

Two recently published reviews, Reappraising striatal D1- and D2-neurons in reward and aversion and Dopamine's Effects on Corticostriatal Synapses during Reward-Based Behaviors, as well as an older review Biological substrates of reward and aversion: A nucleus accumbens activity hypothesis that was appraised in papers involving Berridge(Lateral hypothalamus, nucleus accumbens, and ventral pallidum roles in eating and hunger: interactions between homeostatic and reward circuitry) and Kringlebach (Pleasure systems in the brain) provide some interesting points that I think need to be added to the article. The dichotomy between D1 and D2 expressive MSNs is fairly weak in the NAcc, as activating both can increase motivation, and inhibiting D2 MSNS can reduce motivation. Also, inhibiting NAcc neurons as a whole, whether due to some local excitatory effect(i.e. due to releasing MSNs from massive tonic inhibition) or, as per the classic disinhibition hypothesis, releasing some downstream structure such as the VP or hypothalamus from baseline inhibition, can produce an increase in wanting.Petergstrom (talk) 16:15, 19 April 2018 (UTC)[reply]

I was thinking about adding something along the lines of
"In the dorsal striatum, activation of D1 expressing MSNs produces appetitive incentive salience, while activation of D2 expressing MSNs produces aversive incentive salience. In the NAcc, such a dichotomy is not as clear cut as D2-MSNs do not solely encode aversive motivation.[1][2]"Petergstrom (talk) 16:42, 19 April 2018 (UTC)[reply]
While the optogenetic study provides the most robust contradictory evidence, the pharmacological evidence is slightly confusing, as activation of D2 receptors is putatively inhibitory, and D2 receptor agonism would therefore reduce D2-MSN firing, as would be predicted by a strict dichotomy of D2-indirect and D1-direct pathways in the NAcc.Petergstrom (talk) 17:00, 19 April 2018 (UTC)[reply]
Hmm. The overlap of D1 and D2 expression in MSNs is mainly confined to the NAcc shell; this is consistent with what you've described here though. I haven't read this article, but does the article actually say "incentive salience" or something analogous to "reward motivation", or does it just use the generic term "motivation" as reflected in the quote for this source?[2] In any event, aversive salience and incentive salience are two different things (to be more specific, they're opposing cognitive processes - one mediates attraction, the other mediates avoidance); each is a form of motivational salience though. Seppi333 (Insert 2¢) 19:02, 19 April 2018 (UTC)[reply]
The terminology isn't specific in the Soares-Cunha review, and it uses various terms more or less interchangeably such as “pro-reward”, “anti-reward”, “wanting”, and “incentive salience”, such as in this quotation “This data indicates that both D1R and D2R signalling are relevant for the motivational drive to work to get a food pellet. In fact, using a Pavlovian-to-Instrumental-transfer test (PIT), which indirectly measures “wanting”/incentive salience, it was shown that selective D1R and D2R blockade in the NAc reduced performance”[1]Petergstrom (talk) 19:43, 19 April 2018 (UTC)[reply]
A PIT test demonstrating this is good enough for me so long as the direction of the behavior in both cases was toward obtaining the food. Seppi333 (Insert 2¢) 21:11, 20 April 2018 (UTC)[reply]

References

  1. ^ a b Soares-Cunha, C; Coimbra, B; Sousa, N; Rodrigues, AJ (September 2016). "Reappraising striatal D1- and D2-neurons in reward and aversion". Neuroscience and biobehavioral reviews. 68: 370–386. doi:10.1016/j.neubiorev.2016.05.021. PMID 27235078.
  2. ^ a b Bamford, NS; Wightman, RM; Sulzer, D (7 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. PMID 29420932. Soares-Cunha and coworkers showed that op- togenetic activation of D1R- or D2R-containing SPNs in dorsal striatum both enhance motivation in mice (Soares-Cunha et al., 2016b). Consistent with this, optogenetic inhibition of D2R-con- taining neurons decreases motivation. This study, in agreement with the results obtained with microiontophoresis, suggests that D2R-containing SPNs play a more prominent role in promoting motivation than originally anticipated.

Clinical significance

While most work done in the reward system involves rodent models, and translationally speaking, affective disorders are more difficult to deal with than addiction, I think there is enough research out there on the reward system and affective disorders to include a section in "Clinical Significance". I would probably use Presentation and Neurobiology of Anhedonia in Mood Disorders: Commonalities and Distinctions, Progress in understanding mood disorders:optogenetic dissection of neural circuits, Reconceptualizing anhedonia: novel perspectives on balancing the pleasure networks in the human brain, Emerging role for nucleus accumbens medium spiny neuron subtypes in depression, Reward processing by the lateral habenula in normal and depressive behaviors, Lateral habenula in the pathophysiology of depression, Dopamine System Dysregulation in Major Depressive Disorders, Circuit-based frameworks of depressive behaviors: The role of reward circuitry and beyond.Petergstrom (talk) 17:15, 19 April 2018 (UTC)[reply]

@Petergstrom: Thanks for expanding the article! Be sure to check your additions for typos and unspecified abbreviations when adding content. I've fixed a few typos/abbreviations, but I don't think I caught them all. It'd help if you went over it as well. Seppi333 (Insert 2¢) 23:48, 30 May 2018 (UTC)[reply]
As I was expanding it further, I went through again and tried to clean it up a bit. If there are still any issues, I think it's I'm reading what I intended to write - a second set of eyes would be helpful.Petergstrom (talk) 22:16, 31 May 2018 (UTC)[reply]

Images

@Seppi333: This page is relatively light on images; The only open images I could find are those published in the Castro, Cole and Berridge 2015 article, and I added one under the "wanting" section. So far, attempts to create diagrams myself have been suboptimal.

Basic connectivity based on Zahm/Thompson and Swanson, as well as hedonic hotspots/coldspots
Ventral-Dorsal coordinates lie along the X axis (6.25-8), while Rostral-Caudal coordinates lie along the Y axis(0.5-2.5). The z axis represents the t value from the data scraped from images provided by Pecina and Berridge 2005. The graph on the left represents enhanced liking(Red) and reduced Disgust(Purple), while the right graph represents enhanced liking.

Do you have any ideas, suggestions, or tips?Petergstrom (talk) 09:43, 1 June 2018 (UTC)[reply]

I generally use inkscape to create diagrams since it's a free and commonly used SVG editor; the only other graphical editing software I use is MSPaint (lol) for non-SVG images. I can't really draw diagrams of the brain in it though - my graphics editing skills just aren't on that level. Often, the best approach is to take an existing image and add to/modify it rather than to try to create a new one. The hard part with that is finding the right base image to modify for the intended use. Seppi333 (Insert 2¢) 22:37, 1 June 2018 (UTC)[reply]

Learning

This page contains very little information on the reward system and learning, which is entirely understandable given how the literature tends to approach learning from so many diverse and isolated angels. I'm trying to put together a section, and so far have these papers as potential refs:

@Seppi333: Do you have any suggestions for potential sources?Petergstrom (talk) 22:29, 18 June 2018 (UTC)[reply]

Hmm. Given that "learning" has such an excessively broad topical scope, a lot of the sources in the article could be used to cite at least some statements. E.g., just off the top of my head, reinforcement and classical conditioning are both forms of associative learning, changes in the value/magnitude of incentive salience to stimuli involves learning, and the assignment of incentive salience to a stimulus upon initial exposure to that stimulus involves learning. So the refs in the article that cover incentive salience and classical/operant conditioning in the context of the reward system would probably be your best bet for potential additional sources. Seppi333 (Insert 2¢) 01:27, 19 June 2018 (UTC)[reply]

Clinical evidence of a causal link between dopamine and music-elicited pleasure

Came across this on my newsfeed today, which covers this clinical study: [1]

The form of pleasure that this study involves is a frisson. Need to wait for a review though. Seppi333 (Insert 2¢) 23:56, 24 January 2019 (UTC)[reply]

Article content

A clinical study from January 2019 that assessed the effect of a dopamine precursor (levodopa), antagonist (risperidone), and a placebo on reward responses to music – including the degree of pleasure experienced during musical chills, as measured by changes in electrodermal activity as well as subjective ratings – found that the manipulation of dopamine neurotransmission bidirectionally regulates pleasure cognition (specifically, the hedonic impact of music) in human subjects.[1][non-primary source needed] This research suggests that increased dopamine neurotransmission acts as a sine qua non condition for hedonic reactions to music in humans.[1][non-primary source needed]

References

  1. ^ a b Ferreri L, Mas-Herrero E, Zatorre RJ, Ripollés P, Gomez-Andres A, Alicart H, Olivé G, Marco-Pallarés J, Antonijoan RM, Valle M, Riba J, Rodriguez-Fornells A (January 2019). "Dopamine modulates the reward experiences elicited by music". Proceedings of the National Academy of Sciences of the United States of America. doi:10.1073/pnas.1811878116. 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 (37) and challenges previous findings in animal models on primary rewards, such as food (42, 43). {{cite journal}}: Unknown parameter |lay-date= ignored (help); Unknown parameter |lay-source= ignored (help); Unknown parameter |lay-url= ignored (help)

Wikipedia Ambassador Program course assignment

This article is the subject of an educational assignment at Roosevelt University supported by the Wikipedia Ambassador Program during the 2012 Q3 term. Further details are available on the course page.

The above message was substituted from {{WAP assignment}} by PrimeBOT (talk) on 16:22, 2 January 2023 (UTC)[reply]

arenaplus new comers reward rebate promotion

arenaplus new comers reward rebate promotion 110.54.146.75 (talk) 17:23, 16 February 2024 (UTC)[reply]

Retrieved from "https://mdwiki.org/wiki/Talk:Reward_system"