Talk:Motivational salience

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Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 01:14, 18 January 2022 (UTC)[reply]

Sentence went sideways

https://en.wikipedia.org/w/index.php?title=Incentive_salience&diff=prev&oldid=708804515

As secondary reinforcers drug use, these previously neutral stimuli are assigned incentive salience (which manifests as a craving), sometimes at pathologically high levels, which tranfers to the primary reinforcer (i.e., the use of an addictive drug) with which it was originally paired.

My brain keeps asking "why would secondary reinforcers use drugs?" or "who is 'use' and why would secondary reinforcers drug this creature?" — MaxEnt 04:04, 25 April 2016 (UTC)[reply]

My bad - I omitted a word, so the clause was nonsensical. As secondary reinforcers of drug use, these previously neutral stimuli ... Thanks for pointing that out. Seppi333 (Insert 2¢) 07:24, 25 April 2016 (UTC)[reply]

Refs to add

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References

^ Tibboel H, De Houwer J, Van Bockstaele B (October 2015). "Implicit measures of "wanting" and "liking" in humans". Neurosci. Biobehav. Rev. 57: 350–364. doi:10.1016/j.neubiorev.2015.09.015. PMID 26432503.
^ Koob GF, Volkow ND (August 2016). "Neurobiology of addiction: a neurocircuitry analysis". Lancet Psychiatry. 3 (8): 760–773. doi:10.1016/S2215-0366(16)00104-8. PMID 27475769. Drug addiction represents a dramatic dysregulation of motivational circuits that is caused by a combination of exaggerated incentive salience and habit formation, reward deficits and stress surfeits, and compromised executive function in three stages. The rewarding effects of drugs of abuse, development of incentive salience, and development of drug-seeking habits in the binge/intoxication stage involve changes in dopamine and opioid peptides in the basal ganglia. The increases in negative emotional states and dysphoric and stress-like responses in the withdrawal/negative affect stage involve decreases in the function of the dopamine component of the reward system and recruitment of brain stress neurotransmitters, such as corticotropin-releasing factor and dynorphin, in the neurocircuitry of the extended amygdala. The craving and deficits in executive function in the so-called preoccupation/anticipation stage involve the dysregulation of key afferent projections from the prefrontal cortex and insula, including glutamate, to the basal ganglia and extended amygdala. Molecular genetic studies have identified transduction and transcription factors that act in neurocircuitry associated with the development and maintenance of addiction that might mediate initial vulnerability, maintenance, and relapse associated with addiction. ... Substance-induced changes in transcription factors can also produce competing effects on reward function.¹⁴¹ For example, repeated substance use activates accumulating levels of ΔFosB, and animals with elevated ΔFosB exhibit exaggerated sensitivity to the rewarding effects of drugs of abuse, leading to the hypothesis that ΔFosB might be a sustained molecular trigger or switch that helps initiate and maintain a state of addiction.^141,142

Seppi333 (Insert 2¢) 19:32, 23 September 2016 (UTC)[reply]

Lacking information on Adverse Salience

“Adverse salience“ redirects to this article. While the term is mentioned in the introduction, it is not expanded upon in the article. 74.81.214.90 (talk) 16:54, 10 February 2023 (UTC)[reply]

[Wanting_and_liking_in_humans_review-1] Tibboel H, De Houwer J, Van Bockstaele B (October 2015). "Implicit measures of "wanting" and "liking" in humans". Neurosci. Biobehav. Rev. 57: 350–364. doi:10.1016/j.neubiorev.2015.09.015. PMID 26432503.

[Neurobiology_of_addiction_August_2016_review-2] Koob GF, Volkow ND (August 2016). "Neurobiology of addiction: a neurocircuitry analysis". Lancet Psychiatry. 3 (8): 760–773. doi:10.1016/S2215-0366(16)00104-8. PMID 27475769. Drug addiction represents a dramatic dysregulation of motivational circuits that is caused by a combination of exaggerated incentive salience and habit formation, reward deficits and stress surfeits, and compromised executive function in three stages. The rewarding effects of drugs of abuse, development of incentive salience, and development of drug-seeking habits in the binge/intoxication stage involve changes in dopamine and opioid peptides in the basal ganglia. The increases in negative emotional states and dysphoric and stress-like responses in the withdrawal/negative affect stage involve decreases in the function of the dopamine component of the reward system and recruitment of brain stress neurotransmitters, such as corticotropin-releasing factor and dynorphin, in the neurocircuitry of the extended amygdala. The craving and deficits in executive function in the so-called preoccupation/anticipation stage involve the dysregulation of key afferent projections from the prefrontal cortex and insula, including glutamate, to the basal ganglia and extended amygdala. Molecular genetic studies have identified transduction and transcription factors that act in neurocircuitry associated with the development and maintenance of addiction that might mediate initial vulnerability, maintenance, and relapse associated with addiction. ... Substance-induced changes in transcription factors can also produce competing effects on reward function.¹⁴¹ For example, repeated substance use activates accumulating levels of ΔFosB, and animals with elevated ΔFosB exhibit exaggerated sensitivity to the rewarding effects of drugs of abuse, leading to the hypothesis that ΔFosB might be a sustained molecular trigger or switch that helps initiate and maintain a state of addiction.^141,142

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