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1 Neurobiology of Nutrition Laboratory, Pennington Biomedical Reserarch Center, Louisiana State University System, Baton Rouge, Louisiana, USA
* To whom correspondence should be addressed. E-mail: berthohr{at}pbrc.edu.
Metabolic, cognitive, and environmental factors processed in the forebrain modulate food intake by changing the potency of direct controls of meal ingestion in the brainstem. Here, we behaviorally and anatomically test the role of the hypothalamic proopiomelanocortin system in mediating some of these descending, indirect controls. MTII, a stable MC4/3R agonist injected into the 4th ventricle near the dorsal vagal complex potently inhibited 14-h food intake by decreasing meal size but not meal frequency, and SHU9119, an antagonist increased food intake by selectively increasing meal size. Furthermore, MTII injected into the 4th ventricle increased and SHU9119 tended to decrease heart rate and body temperature measured telemetrically in freely moving rats. Numerous 
-MSH-ir axons were in close anatomical apposition to NTS neurons showing c-Fos in response to gastric distension, expressing neurochemical phenotypes implicated in ingestive control, and projecting to brown adipose tissue. In retrograde tracing experiments, a small percentage of arcuate nucleus POMC neurons was found to project to the dorsal vagal complex. Thus, melanocortin signaling in the brainstem is sufficient to alter food intake through changing the potency of satiety signals and to change sympathetic outflow. Although the anatomical findings support the involvement of hypothalamo-medullary POMC projections in mediating part of the descending, indirect signal, they do not rule out involvement of POMC neurons in the NTS in mediating part of the direct signal.
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