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  • Title: Overnight food deprivation markedly attenuates hindbrain noradrenergic, glucagon-like peptide-1, and hypothalamic neural responses to exogenous cholecystokinin in male rats.
    Author: Maniscalco JW, Rinaman L.
    Journal: Physiol Behav; 2013 Sep 10; 121():35-42. PubMed ID: 23391574.
    Abstract:
    Systemic administration of sulfated cholecystokinin-8 (CCK) activates neurons within the hindbrain nucleus of the solitary tract (NTS) that project directly to the paraventricular nucleus of the hypothalamus (PVN), and these projections underlie the ability of exogenous CCK to activate the hypothalamic-pituitary-adrenal (HPA) stress axis. CCK inhibits food intake, increases NTS neuronal cFos expression, and activates the HPA axis in a dose-dependent manner. While the hypophagic effects of exogenous CCK are attenuated in food-deprived rats, CCK dose-response relationships for NTS and hypothalamic activation in fed and fasted rats are unknown. Within the NTS, noradrenergic A2 and glucagon-like peptide-1 (GLP-1) neurons express cFos after high doses of CCK, and both neuronal populations project directly to the medial parvocellular (mp)PVN. We hypothesized that increasing and correlated proportions of A2, GLP-1, and mpPVN neurons would express cFos in rats after increasing doses of CCK, and that food deprivation would attenuate both hindbrain and hypothalamic neural activation. To test these hypotheses, ad libitum-fed (ad lib) and overnight food-deprived (DEP) rats were anesthetized and perfused with fixative 90min after i.p. injection of 1.0ml saline vehicle containing CCK at doses of 0, 3, or 10μg/kg BW. Additional ad lib and DEP rats served as non-handled (NH) controls. Brain tissue sections were processed for dual immunocytochemical localization of cFos and dopamine-β-hydroxylase to identify A2 neurons, or cFos and GLP-1. Compared to negligible A2 cFos activation in NH control rats, i.p. vehicle and CCK dose-dependently increased A2 activation, and this was significantly attenuated by DEP. DEP also attenuated mpPVN cFos expression across all treatment groups, and A2 activation was strongly correlated with mpPVN activation in both ad lib and DEP rats. In ad lib rats, large and similar numbers of GLP-1 neurons expressed cFos across all i.p. treatment groups, regardless of CCK dose. Surprisingly, DEP nearly abolished baseline GLP-1 cFos expression in NH controls, and also in rats after i.p. injection of vehicle or CCK. We conclude that CCK-induced hypothalamic cFos activation is strongly associated with A2 activation, whereas the relationship between mpPVN and GLP-1 activation is less clear. Furthermore, activation of A2, GLP-1, and mpPVN neurons is significantly modulated by feeding status, suggesting a mechanism through which food intake and metabolic state might impact hypothalamic neuroendocrine responses to homeostatic challenge.
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