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1 Basic Research, Rheoscience, Rodovre, Denmark
2 Northwestern State University, Louisiana Scholars College, Natchioches, LA, USA
3 Neurobiology of Nutrition Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA, USA
* To whom correspondence should be addressed. E-mail: nv{at}rheoscience.com.
A group of neurons in the caudal NTS processes preproglucagon to GLP-1 and GLP-2, peptides that inhibit food intake when administered ICV. The GLP-1/2 containing neural pathways have been suggested to play a role in taste aversion and nausea since LiCl activates these neurons, and LiCl-induced suppression of food intake can be blocked by the GLP-1 receptor antagonist exendin-9. As many gastrointestinal signals related to both satiety and nausea/illness travel via the vagus nerve to the caudal medulla, the present study assessed the capacity of different types of gastric distension (a purely mechanical stimulus) to activate GLP-1 neurons in the caudal NTS. Gastric balloon distension (1.4 mL/min first 5 min, 0.4 mL/min next 5 min, 9 mL total, held for 60 min) in non-anesthetized freely moving rats produced 12- and 17-fold increases in Fos-expressing NTS neurons when distension was mainly in the fundus or corpus, respectively. Fundus and corpus distension increased the percentage of Fos-activated GLP-1 neurons to 21±9% and 32±5% as compared to 1±1% with sham distension (p<0.01). Thus, fundic distension that may be considered within the physiological range activates GLP1/2 containing neurons, suggesting some role in normal satiety. The larger number of activated GLP neurons with mainly corpus distension may indicate its noxious character. The results support the view that the medullary GLP system is involved in appetite control and is activated by stimuli within the behavioral continuum ranging from satiety to nausea.
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