Talk:Reward system

Music neuroscience
Reward system Cognitive control (an only marginally related neuropsychology concept - storing these refs here for now)
 * cites 
 * 
 * Inhibitory control
 * Attention

 Seppi  333  (Insert 2¢) 08:18, 17 August 2015 (UTC) Edited 21:36, 21 July 2016 (UTC)

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)
 * 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.  Seppi  333  (Insert 2¢) 21:50, 15 January 2017 (UTC)
 * 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.  Seppi  333  (Insert 2¢) 21:50, 15 January 2017 (UTC)

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)
 * 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.  Seppi  333  (Insert 2¢) 02:17, 18 January 2017 (UTC)
 * 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)
 * 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.  Seppi  333  (Insert 2¢) 08:19, 18 January 2017 (UTC)
 * 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?  Seppi  333  (Insert 2¢) 00:20, 21 January 2017 (UTC)

Recent content additions
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.


 * 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) and/or this website (see WP:MEDRS).
 * 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 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.  Seppi  333  (Insert 2¢) 09:15, 12 March 2017 (UTC)

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)


 * 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.  "Petergstrom (talk) 16:42, 19 April 2018 (UTC)


 * 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)


 * 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? 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.  Seppi  333  (Insert 2¢) 19:02, 19 April 2018 (UTC)


 * 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” Petergstrom (talk) 19:43, 19 April 2018 (UTC)


 * 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.  Seppi  333  (Insert 2¢) 21:11, 20 April 2018 (UTC)

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)


 * 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.   Seppi  333  (Insert 2¢) 23:48, 30 May 2018 (UTC)


 * 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)

Images
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. Do you have any ideas, suggestions, or tips?Petergstrom (talk) 09:43, 1 June 2018 (UTC)
 * 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.  Seppi  333  (Insert 2¢) 22:37, 1 June 2018 (UTC)

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:
 * Neuronal Reward and Decision Signals: From Theories to Data.
 * Model-based and model-free Pavlovian reward learning: revaluation, revision, and revelation.
 * Dorsal and ventral streams: the distinct role of striatal subregions in the acquisition and performance of goal-directed actions.
 * Reward-guided learning beyond dopamine in the nucleus accumbens: the integrative functions of cortico-basal ganglia networks

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


 * 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.  Seppi  333  (Insert 2¢) 01:27, 19 June 2018 (UTC)

Clinical evidence of a causal link between dopamine and music-elicited pleasure
Came across this on my newsfeed today, which covers this clinical study:

The form of pleasure that this study involves is a frisson. Need to wait for a review though.  Seppi  333  (Insert 2¢) 23:56, 24 January 2019 (UTC)

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. This research suggests that increased dopamine neurotransmission acts as a sine qua non condition for hedonic reactions to music in humans.

Wikipedia Ambassador Program course assignment
This article is the subject of an educational assignment at Roosevelt University supported by the Wikipedia Ambassador Program&#32;during the 2012 Q3 term. Further details are available on the course page.

The above message was substituted from by PrimeBOT (talk) on 16:22, 2 January 2023 (UTC)

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