Abstract
Neuronostatin, a newly identified anorexigenic peptide, is present in the central nervous system. We tested the hypothesis that neuronostatin neurons are activated by feeding as a peripheral factor and that the glutamatergic system has regulatory influences on neuronostatin neurons. The first set of experiments analyzed the activation of neuronostatin neurons by refeeding as a physiological stimulus and the effectiveness of the glutamatergic system on this physiological stimulation. The subjects were randomly divided into three groups: the fasting group, refeeding group, and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)+refeeding group. We found that refeeding increased the phosphorylated signal transducers and transcription activator-5 (pSTAT5) expression in neuronostatin-positive neurons and that the CNQX injection significantly suppressed the number of pSTAT5-expressing neuronostatin neurons. The second set of experiments analyzed the activation pathways of neuronostatin neurons and the regulating effects of the glutamatergic system on neuronostatin neurons. The animals received intraperitoneal injections of glutamate receptor agonists (kainic acid, α-amino-3-hydroxy-5methyl-4-isoazepropionic acid (AMPA), and N-methyl-D-aspartate (NMDA)) or 0.9% NaCl. The number of c-Fos-expressing neuronostatin neurons significantly increased following the AMPA and NMDA injections. In conclusion, we found that the neuronostatin neurons were activated by peripheral or central signals, including food intake and/or glutamatergic innervation, and that the glutamate receptors played an important role in this activation.
Highlights
Neuronostatin (NST), encoded by the somatostatin gene, is an anorexigenic peptide with 16 amino acids [1]
We found that 2-h refeeding after 48-h fasting induced phosphorylated signal transducers and transcription activator-5 expression in neuronostatin neurons of the anterior hypothalamic periventricular nucleus
The injection of specific antagonist CNQX prior to agonist significantly decreased the percentage of phosphorylated signal transducers and transcription activator-5 (pSTAT5)-positive neuronostatin neurons (p < 0.01, Figure 3)
Summary
Neuronostatin (NST), encoded by the somatostatin gene, is an anorexigenic peptide with 16 amino acids [1]. The presence of neuronostatin neurons and neuronostatin-positive axon terminations in the areas of the hypothalamus that control food intake, the demonstration of decreased water and food intake in animals following intraventricular neuronostatin administration, and the decreasing dose-dependent and short-term food intake in mice after intraperitoneal neuronostatin administration all suggest that neuronostatin may play a role in the control of appetite and metabolism [3,4,5]. Brain Sci. 2020, 10, 217; doi:10.3390/brainsci10040217 www.mdpi.com/journal/brainsci. Glutamate-mediated neurotransmission occurs via G-proteinmediated metabotropic and ion channel-forming ionotropic glutamate receptors. These receptors are classified according to their agonists: N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5methyl-4isoazepropionic acid (AMPA), and 2-carboxy-3-carboxymethyl-4-isopropenylpyrrolidine (Kainate) receptors [8]
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