Current perspectives on incentive salience and applications to clinical disorders.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic and theoretical neuroscience without primary clinical data.
PubMed 29503841 · doi:10.1016/j.cobeha.2018.01.007
What was done
This narrative review summarizes affective neuroscience concepts regarding the distinction between 'liking' (hedonic impact) and 'wanting' (incentive salience) and outlines their proposed roles across psychiatric conditions including depression, addiction, and schizophrenia.
What was found
The abstract reports no quantitative metrics or empirical measurements. It highlights that 'liking' is amplified by opioid signaling within discrete limbic sites, while 'wanting' is driven by broader mesocorticolimbic dopamine circuits. Conceptually, incentive salience deficits are linked to avolition, hedonic deficits to anhedonia, excessive salience to addiction, and fearful motivational salience to paranoid symptoms.
Why it matters
Dissociating the neural substrates of motivational wanting from hedonic liking offers a refined framework for understanding and targeting specific symptom domains in psychiatric illness.
Limits
The abstract provides no primary data, sample sizes, or systematic review methodology. The clinical mappings reflect theoretical and mechanistic models rather than direct trial outcomes.
Cited by
- supports Motivational wanting is modulated by dopamine, whereas hedonic liking (pleasure) is mediated by opioid neurotransmitters in the brain rather than dopamine.
- supports Impairment of dopamine circuitry produces profound loss of motivation or apathy, whereas hyperactivation of this circuitry by addictive drugs leads to states of hypermotivation.