Glutamate receptor antagonist suppresses the activation of nesfatin-1 neurons following refeeding or glucose administration

BACKGROUND: Nesfatin-1 is a newly identified satiety peptide that has regulatory effects on food intake and glucose metabolism, and is located in the hypothalamic nuclei, including the supraoptic nucleus (SON). In this study, we have investigated the hypothesis that nesfatin-1 neurons are activated...

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Bibliographic Details
Published in:Folia morphologica 2022, Vol.81 (2), p.379-386
Main Authors: Serter Kocoglu, S., Oy, C., Halk, Z., Cakır, C., Minbay, Z., Eyigor, O.
Format: Article
Language:English
Subjects:
Fasting
Food intake
Glucose
Glucose metabolism
Glutamatergic transmission
Glutamic acid receptors
Hypothalamus
Injection
Laboratory testing
Metabolism
Neurons
Physiology
Satiety
Supraoptic nucleus
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Summary:BACKGROUND: Nesfatin-1 is a newly identified satiety peptide that has regulatory effects on food intake and glucose metabolism, and is located in the hypothalamic nuclei, including the supraoptic nucleus (SON). In this study, we have investigated the hypothesis that nesfatin-1 neurons are activated by refeeding and intraperitoneal glucose injection and that the glutamatergic system has regulatory influences on nesfatin-1 neurons in the SON. MATERIALS AND METHODS: The first set of experiments analysed activation of nesfatin-1 neurons after refeeding as a physiological stimulus and the effectiveness of the glutamatergic system on this physiological stimulation. The subjects were randomly divided into three groups: fasting group, refeeding group and antagonist (CNQX + refeeding) group. The second set of experiments analysed activation of nesfatin-1 neurons by glucose injection as a metabolic stimulus and the effectiveness of the glutamatergic system on this metabolic stimulation. The subjects were randomly divided into three groups: saline group, glucose group and antagonist (CNQX + glucose) group. RESULTS: Refeeding significantly increased the number of activated nesfatin-1 neurons by approximately 66%, and intraperitoneal glucose injection activated these neurons by about 55%, compared to the fasting and saline controls. The injections of glutamate antagonist (CNQX) greatly decreased the number of activated nesfatin-1 neurons. CONCLUSIONS: This study suggested that nesfatin-1 neurons were activated by peripheral and/or metabolic signals and that this effect was mediated through the glutamatergic system.
ISSN:0015-5659
1644-3284
DOI:10.5603/FM.a2021.0034