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Reward system
Cognitive control (an only marginally related neuropsychology concept - storing these refs here for now)
Reflist
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References
|
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)
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)
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)
@ 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
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)
References
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.
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)
@ 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.
Do you have any ideas, suggestions, or tips? Petergstrom ( talk) 09:43, 1 June 2018 (UTC)
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)
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)
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
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).
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arenaplus new comers reward rebate promotion 110.54.146.75 ( talk) 17:23, 16 February 2024 (UTC)
This is the
talk page for discussing improvements to the
Reward system article. This is not a forum for general discussion of the article's subject. |
Article policies
|
Find medical sources: Source guidelines · PubMed · Cochrane · DOAJ · Gale · OpenMD · ScienceDirect · Springer · Trip · Wiley · TWL |
Archives: 1 |
![]() | Ideal sources for Wikipedia's health content are defined in the guideline
Wikipedia:Identifying reliable sources (medicine) and are typically
review articles. Here are links to possibly useful sources of information about Reward system.
|
![]() | The contents of the Pleasure center page were merged into Reward system. For the contribution history and old versions of the redirected page, please see its history; for the discussion at that location, see its talk page. |
![]() | This article is rated C-class on Wikipedia's
content assessment scale. It is of interest to the following WikiProjects: | |||||||||||||||||||||||||||||||||||||||||||
|
Reward system
Cognitive control (an only marginally related neuropsychology concept - storing these refs here for now)
Reflist
|
---|
References
|
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)
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)
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)
@ 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
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)
References
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.
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)
@ 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.
Do you have any ideas, suggestions, or tips? Petergstrom ( talk) 09:43, 1 June 2018 (UTC)
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)
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)
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
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)
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)
arenaplus new comers reward rebate promotion 110.54.146.75 ( talk) 17:23, 16 February 2024 (UTC)