Peripheral glucagon-like-peptide-1 receptor (GLP-1R) activation engages a set of physiological responses that include inhibition of gastric emptying (GE). Does peripheral or central GLP-1R activation mediate the GE response? Previous reports and data from our laboratory suggest that inhibition of GE by GLP-1R is mediated by peripheral receptors the engage central processing via vagal afferents. Support for this view comes from surgical and chemical lesioning of the vagus and from targeted central application of GLP-1R antagonist in conjunction with intraperitoneal (IP) delivery of the selective GLP-1R agonist Exendin-4. Here we determined whether forebrain processing is required for GE response production by investigating the dose-response function of IP Exendin-4 on GE rates of chronic supracollicular decerebrate (CD) rats in comparison to neurologically intact control rats. In both control and CD rats, the lowest dose of Exendin-4 (0.12 μg/kg) was ineffective in altering GE rates (72.0±3.9 and 62.4±5.5%) compared to vehicle (73.5±1.9 and 69.8±1.5%), whereas a dose of 1.2 μg/kg similarly suppressed GE in control and CD rats (43.2±6.1 and 46.6±5.5%). Significant suppression, but no further enhancement occurred at the highest dose of Exendin-4 (2.4 μg/kg) in control and CD rats (53.5±4.2 and 50.9±2.4%). These studies demonstrate that the caudal brainstem is sufficient to mediate GLP-1R-mediated inhibition of GE and that forebrain processing is not required. Support by DK21397.