Central nesfatin-1-expressing neurons are sensitive to peripheral inflammatory stimulus |
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Authors: | Marion S Bonnet Emilie Pecchi Jér?me Trouslard André Jean Michel Dallaporta Jean-Denis Troadec |
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Institution: | 1. Centre de Recherche en Neurobiologie-Neurophysiologie de Marseille (CRN2M), UMR 6231 CNRS, Marseille, France 2. Département de Physiologie Neurovégétative, USC INRA 2027, Université Paul Cézanne, Université de la Méditerranée, Marseille, France
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Abstract: | Recently, a novel factor with anorexigenic properties was identified and called nesfatin-1. This protein (82 aac) is not only
expressed in peripheral organs but it is also found in neurons located in specific structures including the hypothalamus and
the brainstem, two sites strongly involved in food intake regulation. Here, we studied whether some of the neurons that become
activated following an injection of an anorectic dose of lipopolysaccharides (LPS) exhibit a nesfatin-1 phenotype. To this
end, we used double immunohistochemistry to target the expression of the immediate-early gene c-fos and of nesfatin-1 on coronal frozen sections of the rat brain. The number of c-Fos+/nesfatin-1+ neurons was evaluated in
the immunosensitive structures reported to contain nesfatin-1 neurons; i.e. paraventricular hypothalamic nucleus (PVN), supraoptic
nucleus (SON), arcuate nucleus (ARC) and nucleus of the solitary tract (NTS). LPS strongly increased the number of c-Fos+/nesfatin-1+
neurons in the PVN, SON and NTS, and to a lesser extent in the ARC. Triple labeling showed that a portion of the nesfatin-1
neurons activated in response to LPS within the NTS are catecholaminergic since they co-express tyrosine hydroxylase (TH).
Our data therefore indicate that a portion of nesfatin-1 neurons of both the hypothalamus and brainstem are sensitive to peripheral
inflammatory signals, and provide the first clues suggesting that centrally released nesfatin-1 may contribute to the neural
mechanisms leading to endotoxaemic anorexia. |
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