Serotonin and Dopamine Mimic Glucose-Induced Reinforcement in C. elegans : Potential Role of NSM Neurons and the Serotonin Subtype 4 Receptor.

Autor:	Schwartz EKC; Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States., Sosner EN; Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States., Desmond HE; Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States., Lum SJ; Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States., Sze JY; Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY, United States., Mobbs CV; Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States.
Jazyk:	angličtina
Zdroj:	Frontiers in physiology [Front Physiol] 2021 Dec 20; Vol. 12, pp. 783359. Date of Electronic Publication: 2021 Dec 20 (Print Publication: 2021).
DOI:	10.3389/fphys.2021.783359
Abstrakt:	Food produces powerful reinforcement that can lead to overconsumption and likely contributes to the obesity epidemic. The present studies examined molecular mechanisms mediating food-induced reinforcement in the model system C. elegans . After a 1-h training session during which food (bacteria) is paired with the odorant butanone, odor preference for butanone robustly increased. Glucose mimicked this effect of bacteria. Glucose-induced odor preference was enhanced similarly by prior food withdrawal or blocking glucose metabolism in the presence of food. Food- and glucose-induced odor preference was mimicked by serotonin signaling through the serotonin type-4 (5-HT4) receptor. Dopamine (thought to act primarily through a D1-like receptor) facilitated, whereas the D2 agonist bromocriptine blocked, food- and glucose-induced odor preference. Furthermore, prior food withdrawal similarly influenced reward produced by serotonin, dopamine, or food, implying post-synaptic enhancement of sensitivity to serotonin and dopamine. These results suggest that glucose metabolism plays a key role in mediating both food-induced reinforcement and enhancement of that reinforcement by prior food withdrawal and implicate serotonergic signaling through 5-HT4 receptor in the re-enforcing properties of food. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2021 Schwartz, Sosner, Desmond, Lum, Sze and Mobbs.)
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu