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| Several studies have implicated the dorsomedial hypothalamic nucleus (DMN) in regulation of feeding behavior and body weight, but clear mechanisms by which it controls food intake are not well understood. Here we report that DMN received important peripheral short-term and long-term feeding-related afferent signals, including the gastric vagal inputs, glycemia, cholecystokinin (CCK) as well as leptin, an adipostatic signal forcefully inhibiting food intake and increasing metabolic rate. Among the 279 DMN neurons recorded, 173 (62.0%) responded to the stimulation of gastric vagal nerves. Also, of the 123 DMN neurons responsive to the gastric vagal stimulation that tested for intravenous glucose administration, 75 (61.0%) were identified to be glycemia-sensitive. Moreover, it is noteworthy that within the 23 DMN neurons responding to both of the gastric vagal and intravenous glucose stimulations, most cells (19/23, 82.6%) were sensitive to circulating leptin and some neurons (n = 7) were also responsive to systemic CCK, suggesting gastric vagal, glycemic, CCK and leptin inputs converge onto single DMN neurons. Furthermore, synergistic interactions between leptin and glucose on single DMN neurons were observed (n = 6). These results demonstrate that those important peripheral feeding-related gastric vagal, glycemic, CCK and leptin signals not only reach the DMN but also interact on single DMN neurons, suggesting that the DMN may not just function as a relay station, but independently integrate the short-term and long-term feeding-associated information and actively participate in the direct regulation of feeding behavior. |
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| Keywords:dorsomedial hypothalamic nucleus; leptin; gastric vagal nerves; glycemia-sensitive neurons; feeding regulation |
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