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Background & Aims: To observe the effects ofnesfatin-1 on the glucosensing neurons in the nucleus of solitary tract (NTS), explore the mechanism of NTS neurons involved in the suppressing of food intake.Methods:Whole-cell patch-clamp technique was used to record the discharges of 30 neurons in the NTS slice before and after the administration of glucose and nesfatin-l.Results: The 30 NTS neurons were tested with glucose, of which 13 were activated and identified as glucose-excited (G-E) neurons.The firing rate of G-E significantly increased from (0.63±0.2) Hz to (1.73±0.52) Hz (P<0.05) after glucose administration (5 mM).Of which 5 were depressed by glucose and identified as glucose-inhibited (G-I) neurons;The firing rate of G-I neurons significantly reduced from (2.74±0.08) Hz to (0.63±0.18) Hz (P<0.01) after glucose administration.Of which 12 failed to respond to glucose.10min after retuming to normal ACSF, 13 G-E neurons were examined for response to nesfatin-l (10 nM), 12 were activated from (1.24±0.40) Hz to (3.40±0.82) Hz (P<0.01), and 1 failed to respond to nesfatin-1.4 out of 5 G-I neurons were suppressed by nesfatin-1 from (2.67±0.41) Hz to (0.71±0.14) Hz (P<0.05), and 1 failed to respond to nesfatin-l.Conclusion: Our data demonstrated that this newly-discovered peptide may exert at least a part of its physiological actions on the control of food intake as a direct result of its role in controlling the excitability of neurons in the NTS.