According to the World Health Organization, there were over 340 million obese or overweight children and adolescents worldwide in 2016. Western diet consumption, based on refined sugars and high-fat foods, leads to obesity and negative effects on the brain, resulting in cognitive impairments even before changes in body weight. This is especially concerning for young people, since brain development, neurogenic processes, and neuronal maturation occur during this life period. Knowing this, our study aimed to analyze the effects of high-caloric diets on the hippocampus, particularly on the gamma-amino-butyric acid (GABA)ergic system, and its relation with the cholinergic system, neurogenesis, and neuroinflammation. We compared the effects of two different high-caloric diets administered to juvenile rats for 12 weeks, one diet rich in sugar (30% sucrose liquid solution), and a cafeteria diet, rich in sugar and high-fat foods. The cafeteria diet reduced the density of parvalbumin (PV) positive neurons in the granular layer, hilus, and CA1, and of neuropeptide Y (NPY) positive neurons in the hilus. The high-sugar diet decreased the density of PV-positive cells in CA3. The cafeteria diet also reduced the mRNA relative expression of reelin (RELN) and increased the number, but reduced the length, of the astrocyte processes. In conclusion, these results highlight the significance of determining the mechanisms mediating the observed effects of these diets and imply that the cognitive impairments, previously found in a vulnerable period, might be related to both the neuroinflammation process, and the reduction of PV, NPY, and RELN expression in the hippocampal formation.