Background: Eating behaviour is regulated by a lot of signals that are produced in the gastrointestinal (GI) tract which act directly on the brain via circumventricular organs and/or are conveyed by vagal afferents to neurons of the nucleus of the solitary tract (NST), which project to areas involved in controlling food intake, like the hypothalamus. Oleoylethanolamide (OEA), a lipid messenger produced by the enterocytes upon the ingestion of fat, reduces food intake and body weight in rodents and is associated with c-fos induction in brain areas such as the NST, the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei. (Gaetani et al., 2010) Previous studies demonstrate that OEA increases the brain noradrenergic transmission (Romano et al., 2013) and that the effects of OEA are abolished in rats subjected to total subdiaphragmatic vagotomy or treated with capsaicin. (De Fonseca, 2001) In this study we investigate the role of abdominal vagal afferents in mediating the effects induced by OEA administration. Methods: Rats were subjected to subdiaphragmatic vagal deafferentation (SDA), a surgical procedure that eliminates all abdominal vagal afferents but leaves about 50% of the vagal efferents intact. SHAM-operated rats were used as control. SDA and SHAM-operated rats were subjected to peripheral administration of OEA (10mg/Kg) and their brains were collected for immunohistochemical analyses. Fos expression was evaluated at both brainstem (NTS and area postrema AP) and hypothalamic level. Moreover, dopamine-β-hydroxylase (DBH) expression in NTS was evaluated. Results: Our behavioural results showed that OEA decreased food intake in both SDA and SHAM rats Semiquantitative analyses obtained by immunohistochemistry experiments revealed that the ablation of vagal afferents did not affect the capability of OEA to increase Fos expression within the brainstem or the PVN. Also DBH pattern expression within NST subnuclei was not affected by SDA surgery. Conclusions: Vagal afferents aren’t strictly necessary for the effect of OEA on satiety and brain activation. Interestingly the high expression of Fos observed at the level of the AP in the SDA rats is in accordance with our recent results demonstrating that neurons of the AP are crucially involved in mediating both behavioural and neurochemical effect of OEA, suggesting the hypothesis that OEA could reach the central nervous system through a dual mechanism, which involves both afferent fibers and AP neurons.

"EFFECTS OF SUBDIAPHRAGMATIC DEAFFERENTATION ON OLEOYLETHANOLAMIDE INDUCED FOS EXPRESSION IN THE BRAIN" / de Ceglia, M.; Koczwara, J. B.; Gallelli, C. A.; Azari, E. K.; Arnold, M.; Romano, A.; Gaetani, S.. - (2018). (Intervento presentato al convegno 21st SIF SEMINAR tenutosi a Milano).

"EFFECTS OF SUBDIAPHRAGMATIC DEAFFERENTATION ON OLEOYLETHANOLAMIDE INDUCED FOS EXPRESSION IN THE BRAIN"

M. de Ceglia;J. B. Koczwara;C. A. Gallelli;A. Romano;S. Gaetani
2018

Abstract

Background: Eating behaviour is regulated by a lot of signals that are produced in the gastrointestinal (GI) tract which act directly on the brain via circumventricular organs and/or are conveyed by vagal afferents to neurons of the nucleus of the solitary tract (NST), which project to areas involved in controlling food intake, like the hypothalamus. Oleoylethanolamide (OEA), a lipid messenger produced by the enterocytes upon the ingestion of fat, reduces food intake and body weight in rodents and is associated with c-fos induction in brain areas such as the NST, the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei. (Gaetani et al., 2010) Previous studies demonstrate that OEA increases the brain noradrenergic transmission (Romano et al., 2013) and that the effects of OEA are abolished in rats subjected to total subdiaphragmatic vagotomy or treated with capsaicin. (De Fonseca, 2001) In this study we investigate the role of abdominal vagal afferents in mediating the effects induced by OEA administration. Methods: Rats were subjected to subdiaphragmatic vagal deafferentation (SDA), a surgical procedure that eliminates all abdominal vagal afferents but leaves about 50% of the vagal efferents intact. SHAM-operated rats were used as control. SDA and SHAM-operated rats were subjected to peripheral administration of OEA (10mg/Kg) and their brains were collected for immunohistochemical analyses. Fos expression was evaluated at both brainstem (NTS and area postrema AP) and hypothalamic level. Moreover, dopamine-β-hydroxylase (DBH) expression in NTS was evaluated. Results: Our behavioural results showed that OEA decreased food intake in both SDA and SHAM rats Semiquantitative analyses obtained by immunohistochemistry experiments revealed that the ablation of vagal afferents did not affect the capability of OEA to increase Fos expression within the brainstem or the PVN. Also DBH pattern expression within NST subnuclei was not affected by SDA surgery. Conclusions: Vagal afferents aren’t strictly necessary for the effect of OEA on satiety and brain activation. Interestingly the high expression of Fos observed at the level of the AP in the SDA rats is in accordance with our recent results demonstrating that neurons of the AP are crucially involved in mediating both behavioural and neurochemical effect of OEA, suggesting the hypothesis that OEA could reach the central nervous system through a dual mechanism, which involves both afferent fibers and AP neurons.
2018
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1352000
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