Talk:Reward system

• ^[1]  Added

Reward system

• ^[2] cites ^[3]
• ^[4]
• ^[5]

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

• Inhibitory control^[6]
• Attention^[7]

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

''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. Seppi333 (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. Seppi333 (Insert 2¢) 21:50, 15 January 2017 (UTC)

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. Seppi333 (Insert 2¢) 02:17, 18 January 2017 (UTC)

@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)

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)

@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)

@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)

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.^[1][2]"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?^[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)

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)

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)