ReviewPhysiology & behavior2017
Physiological state tunes mesolimbic signaling: Lessons from sodium appetite and inspiration from Randall R. Sakai.
Review in Physiology & behavior, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Separating desire from prediction of outcome value.Trends in cognitive sciences · 2023Review
- Thirst recruits phasic dopamine signaling through subfornical organ neurons.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Sodium Imbalance in Mice Results Primarily in Compensatory Gene Regulatory Responses in Kidney and Colon, but Not in Taste Tissue.Nutrients · 2020Article
- FGF21 and the Physiological Regulation of Macronutrient Preference.Endocrinology · 2020Review
- The Functional and Neurobiological Properties of Bad Taste.Physiological reviews · 2019Review
- Parallels and Overlap: The Integration of Homeostatic Signals by Mesolimbic Dopamine Neurons.Frontiers in psychiatry · 2018Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Sodium deficit poses a life-threatening challenge to body fluid homeostasis and generates a sodium appetite - the behavioral drive to ingest sodium. Dr. Randall R. Sakai greatly contributed to our understanding of the hormonal responses to negative sodium balance and to the central processing of these signals. Reactivity to the taste of sodium solutions and the motivation to seek and consume sodium changes dramatically with body fluid balance. Here, we review studies that collectively suggest that sodium deficit recruits the mesolimbic system to play a role in the behavioral expression of sodium appetite. The recruitment of the mesolimbic system likely contributes to intense sodium seeking and reinforces sodium consumption observed in deficient animals. Some of the hormones that are released in response to sodium deficit act directly on both dopamine and nucleus accumbens elements. Moreover, the taste of sodium in sodium deficient rats evokes a pattern of dopamine and nucleus accumbens activity that is similar to responses to rewarding stimuli. A very different pattern of activity is observed in non-deficient rats. Given the well-characterized endocrine response to sodium deficit and its central action, sodium appetite becomes an ideal model for understanding the role of mesolimbic signaling in reward, reinforcement and the generation of motivated behavior.
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Registered trials
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