Growing evidence indicates that glial plasticity plays a role in feeding control, by adapting neuronal transmission to metabolic needs. Astroglial morphological changes and microglial activation occurs in response to feeding, in the hypothalamus and in other brain area involved in feeding regulation such as the olfactory bulb. Glial plasticity seems to evolve to glial activation in response to high-fat-high-sugar western diets (WD) consumption generating pro-inflammatory/obesogenic states. There is an abundant glial population in the dorsal vagal complex (DVC), a brainstem area involved in the integration of digestive signals. A thick border of astrocytes delineates the area postrema (AP), a circumventricular organ with permeable blood barrier, from the nucleus of the tractus solitarius (NTS) homing neuronal species involved in satiety, and astrocytes. Microglia are also abundant in the AP and NTS, where pro-inflammatory signals may arrive from the gut in response to dietary load and digestion. However, little is known about the involvement of these glial populations in the satietogenic signals from the DVC. Our aim was to evaluate astrocytes and microglial changes in response to chronic or repeated episodes of western diet in the DVC of rats or mice. We have analysed the extent of the astrocyte spreading and the number and morphological phenotype of microglia in the AP and NTS by immunohistochemistry, on two rodent models: rats submitted to a high-fat/high-sugar diet (WD), and mice submitted to several 1-week-episodes of WD. Brainstems were taken after killing, fixed in formalin, and cryostat-cut coronal sections were labelled and analysed for astrocytes (GFAP) and microglia (Iba1). We found an increase in the astrocyte spreading (GFAP labelled area and thickness) between the AP and the NTS (but not in the astrocytes within the NTS) after one month of WD in rats as well as in mice after the repeated episodes of WD, as compared to control animals. We did not observe any increase in the microglial number or morphology within the AP in WD fed animals whereas we found an increased number of microglial cells in the NTS of WD fed rats as compared to controls. These glial changes were associated with several digestive markers alteration.These results show morphological changes enlarging the astroglial barrier between the AP and NTS in the DVC of rodents receiving a western diet. This was observed after a chronic exposition in rats or repeated expositions in mice, suggesting a persistence of the influence of the diet on the size of the astroglial barrier. Such an astroglial morphological plasticity in the DVC, between the AP and the NTS, may play a role in the adaptation of the satietogenic activity of the neurons to the type of diet.