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G. Cristina Brailoiu, Siok L. Dun, Eugen Brailoiu, Saadet Inan, Jun Yang, Jaw Kang Chang, Nae J. Dun, Nesfatin-1: Distribution and Interaction with a G Protein-Coupled Receptor in the Rat Brain, Endocrinology, Volume 148, Issue 10, 1 October 2007, Pages 5088–5094, https://doi.org/10.1210/en.2007-0701
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Nesfatin-1 is a recently identified satiety molecule detectable in neurons of the hypothalamus and nucleus of solitary tract (NTS). Immunohistochemical studies revealed nesfatin-1-immunoreactive (irNEF) cells in the Edinger-Westphal nucleus, dorsal motor nucleus of vagus, and caudal raphe nuclei of the rats, in addition to the hypothalamus and NTS reported in the initial study. Double-labeling immunohistochemistry showed that irNEF cells were vasopressin or oxytocin positive in the paraventricular and supraoptic nucleus; cocaine-amphetamine-regulated transcript or tyrosine hydroxylase positive in arcuate nucleus; cocaine-amphetamine-regulated transcript or melanin concentrating hormone positive in the lateral hypothalamus. In the brainstem, irNEF neurons were choline acetyltransferase positive in the Edinger-Westphal nucleus and dorsal motor nucleus of vagus; tyrosine hydroxylase positive in the NTS; and 5-hydroxytryptamine positive in the caudal raphe nucleus. The biological activity of rat nesfatin-1 (1–82) (100 nm) was assessed by the Ca2+ microfluorometric method. Nesfatin-1 elevated intracellular Ca2+ concentrations [Ca2+]i in dissociated and cultured hypothalamic neurons. The response was prevented by pretreating the cells with pertussis toxin (100 nm) or Ca2+-free solution and by a combination of the L-type and P/Q-type calcium channel blocker verapamil (1 μm) and omega-conotoxin MVIIC (100 nm). The protein kinase A inhibitor KT 5720 (1 μm) suppressed nesfatin-1-induced rise in [Ca2+]i. The result shows that irNEF is distributed to several discrete nuclei in the brainstem, in addition to the hypothalamus and NTS reported earlier, and that the peptide interacts with a G protein-coupled receptor, leading to an increase of [Ca2+]i, which is linked to protein kinase A activation in cultured rat hypothalamic neurons.
