Brainstem metabotropic glutamate receptors reduce food intake and activate dorsal pontine and medullar structures after peripheral bacterial lipopolysaccharide administration.

Léa Chaskiel, Flora Paul, Rüdiger Gerstberger, Thomas Hübschle, Jan Pieter Konsman
Neuropharmacology. 2016-08-01; 107: 146-159
DOI: 10.1016/j.neuropharm.2016.03.030

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1. Neuropharmacology. 2016 Aug;107:146-159. doi: 10.1016/j.neuropharm.2016.03.030.
Epub 2016 Mar 22.

Brainstem metabotropic glutamate receptors reduce food intake and activate dorsal
pontine and medullar structures after peripheral bacterial lipopolysaccharide
administration.

Chaskiel L(1), Paul F(1), Gerstberger R(2), Hübschle T(2), Konsman JP(3).

Author information:
(1)CNRS, PsychoNeuroImmunologie, Nutrition et Génétique, UMR 5226, Bordeaux,
France; Univ. Bordeaux, PsyNuGen, UMR 5226, Bordeaux, France.
(2)Institut für Veterinär-Physiologie und -Biochemie, Justus-Liebig-Universität
Giessen, 35392 Giessen, Germany.
(3)CNRS, PsychoNeuroImmunologie, Nutrition et Génétique, UMR 5226, Bordeaux,
France; Univ. Bordeaux, PsyNuGen, UMR 5226, Bordeaux, France. Electronic address:
.

During infection-induced inflammation food intake is reduced. Vagal and brainstem
pathways are important both in feeding regulation and immune-to-brain
communication. Glutamate is released by vagal afferent terminals in the nucleus
of the solitary tract and by its neurons projecting to the parabrachial nuclei.
We therefore studied the role of brainstem glutamate receptors in spontaneous
food intake of healthy animals and during sickness-associated hypophagia after
peripheral administration of bacterial lipopolysaccharides or interleukin-1beta.
Brainstem group I and II metabotropic, but not ionotropic, glutamate receptor
antagonism increased food intake both in saline- and lipopolysaccharide-treated
rats. In these animals, expression of the cellular activation marker c-Fos in the
lateral parabrachial nuclei and lipopolysaccharide-induced activation of the
nucleus of the solitary tract rostral to the area postrema were suppressed. Group
I metabotropic glutamate receptors did not colocalize with c-Fos or neurons
regulating gastric function in these structures. Group I metabotropic glutamate
receptors were, however, found on raphé magnus neurons that were part of the
brainstem circuit innervating the stomach and on trigeminal and hypoglossal motor
neurons. In conclusion, our findings show that brainstem metabotropic glutamate
receptors reduce food intake and activate the lateral parabrachial nuclei as well
as the rostral nucleus of the solitary tract after peripheral bacterial
lipopolysaccharide administration. They also provide insight into potential group
I metabotropic glutamate receptor-dependent brainstem circuits mediating these
effects.

Copyright © 2016 Elsevier Ltd. All rights reserved.

DOI: 10.1016/j.neuropharm.2016.03.030
PMID: 27016016 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus