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Taste reactivity analysis of 6-hydroxydopamine-induced aphagia: Implications for arousal and anhedonia hypotheses of dopamine function.
Abstract
The deficits in feeding and drinking that result from 6-hydroxydopamine (6-OHDA) lesions of the mesostriatal dopamine system are often explained using either sensorimotor arousal or anhedonia hypotheses. Sensorimotor arousal hypotheses posit that dopamine systems facilitate the capacity of sensory stimuli to activate any motor output. The anhedonia hypothesis suggests that dopamine systems amplify the hedonic impact of positive reinforcers. Natural palatability-dependent ingestive and aversive actions, which are emitted by rats to tastes, provide a sensitive test that can discriminate between these hypotheses: A reduction of sensorimotor arousal should diminish the ability of tastes to elicit any actions, whereas anhedonia should shift the balance between positive and aversive actions. To directly compare these two hypotheses, taste reactivity was examined in rats made aphagic by intranigral 6-OHDA injections. The results did not support either of these predictions: Taste reactivity was essentially unchanged. The persistence of normal taste reactivity argues against both an anhedonia and a global sensorimotor arousal interpretation and provides further evidence that the capacity for hedonics can be neurologically dissociated from motivated appetitive behavior. An incentive attribution hypothesis that can account for the results is discussed, along with its implications for a wide range of phenomena associated with dopamine depletion.
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“Further, even complete removal of nearly all dopamine by neurochemical brain lesions left rats’ sweetness ‘liking’ completely normal and unimpaired, despite eliminating all ‘wanting’ to eat (Berridge et al., 1989).”
From Evolving Concepts of Emotion and Motivation (2018) · cites this paper as Berridge et al., 1989
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Metadata
- Authors
- Berridge, K. C., Venier, I. L., & Robinson, T. E.
- Affiliations
- University of Michigan (US)
- Venue
- Behavioral Neuroscience
- Published
- 1989-02
- Volume
- 103
- Issue
- 1
- Pages
- 36-45
- ISSN
- 0735-7044 (ISSN-L)
- 1939-0084
- OpenAlex
- W4239398105
- Cited by
- 356
- References
- 0
- Citations by year
- 2026: 2 · 2025: 14 · 2024: 12 · 2023: 19 · 2022: 12 · 2021: 6 · 2020: 54 · 2019: 42 · 2018: 9 · 2017: 8 · 2016: 10 · 2015: 11 · 2014: 2 · 2013: 7 · 2012: 12
- FWCI
- 2.84
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Behavioral Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Mental Health (MH-37277)
- National Institute of Neurological Disorders and Stroke (NS-23959)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Sensory Systems › Olfactory and Sensory Function Studies
- Keywords
- 6-hydroxydopamine, aphagia, taste reactivity, dopaminergic activity, arousal hypothesis, dopamine depletion, dietary intake
- MeSH terms
- Animals, Feeding and Eating Disorders, Arousal, Dopamine, Hydroxydopamines, Male, Rats, Inbred Strains, Taste, Oxidopamine, Rats
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