Endocrine Abstracts (2010) 22 P603

Adrenalectomy (ADX) increases the activation of hypothalamic and nucleus of the solitary tract (NTS) neurons related with food intake control during endotoxemia

Rodrigo Rorato, Ernane Uchoa, Jose Antunes-Rodrigues & Lucila Elias

School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Sao Paulo, Brazil.

Endotoxemia induces behavioral changes, including a decrease of food intake. Several studies have demonstrated that ADX modifies central nervous system responsiveness to different paradigms. Control of energy homeostasis is regulated by interplay of peripheral signaling conveyed to the hypothalamus and brainstem that control appetite and meal size. We investigated the activity of oxytocin (OT) neurons in the paraventricular nucleus of the hypothalamus (PVN) and tyrosine hydroxylase (TH) neurons in the NTS, both related with control of food intake, after lipopolysaccharide (LPS, 100 μg/kg, i.p.) or saline injection in ADX and sham rats. Food intake was determined 4 h after injections. Another set of rats was transcardially perfused 4 h after injections for brain collection and subsequent immunohistochemistry of hypothalamic slices. ADX rats showed lower food intake, compared with sham, both after saline and LPS treatment. We observed that LPS treatment increased Fos and Fos/OT neurons in the medial parvocellular subdivision of the PVN in sham rats (Fos: 19.2±4.1 and Fos/OT: 2.6±1.3) and this response was enhanced in ADX rats (Fos: 61±17 and Fos/OT: 8.5±3.7). In the posterior parvocellular subdivision of the PVN, an increased Fos and Fos/OT double labeled neurons after LPS was observed only in ADX rats (Fos: 7.7±3.4 and Fos/OT: 2.0±0.9). LPS treatment increased Fos and Fos/TH double labeled neurons in the NTS only in the ADX rats (Fos: 34.7±13 and Fos/TH: 6.1±0.6). In conclusion, adrenalectomy enhances hypophagia during endotoxemia and this effect is associated with an increased activation of hypothalamic and NTS pathways, mediated by oxytocinergic and catecholaminergic neurons.

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