Recent indications are suggesting that high fat and sugar-enriched foods do not only evoke harmful physiological conditions, but they also endure evident structural alterations in cerebral regions controlling cognitive and feeding behaviors. Food consumption plus neuronal energy regulatory mechanisms seem to constitute a complex system assuring that food calories do not exceed body requirements. At the same time obesogenic-related properties of limbic feeding stations like the hypothalamus (HTH), hippocampus (HIP) and amygdala (AMY) tend to control eating habits through the interaction of distinct neuropeptides. For this purpose, it was our intention to correlate expression differences of a key anti-obesogenic neuropeptide receptor i.e. neurotensin1 (NTR1) on mnemonic performances in the hibernating hamster (Mesocricetus auratus) exposed to a high fat diet (HFD). Interestingly, these hamsters exhibited a notable enhanced (p < 0.01) body weight from the fifth on to the twelfth week of treatment, which was accompanied by elevated blood lipid cholesterolo and triglycerides and glucose levels. At the same time these hamsters provided diminished locomotor activities such as exploratory bouts, rearing and grooming behaviors. Of greater relevance was their very extreme (p < 0.001) inability of identifying new objects during novel object recognition (NOR) tests along with not having correctly chosen the chamber of the conditioned place preference (CPP) apparatus, which contained the gratifying reward. Surprisingly the altered behavioral plus mnemonic tasks of HFD hamsters were tightly related to elevated NTR1 expression changes in the above limbic sites thus proposing this neuronal system as a highly probable alternative for treating obesity-dependent mnemonic dysfunctions.