Fazzari Gilda, Zizza Merylin, Di Vito Anna, Alò Raffaella, Mele Maria, Bruno Rosalinda, Barni Tullio, Facciolo Rosa Maria, Canonaco Marcello
Comparative Neuroanatomy Laboratory of Biology, Ecology and Earth Science Department (DiBEST), University of Calabria, Ponte P. Bucci 4B, 87036, Arcavacata di Rende, Cosenza, Italy.
Department of Clinical and Experimental Medicine, University of Catanzaro "Magna Græcia", Viale Europa, 88100, Catanzaro, Italy.
Behav Brain Res. 2018 Jul 16;347:227-233. doi: 10.1016/j.bbr.2018.03.015. Epub 2018 Mar 13.
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.
近期迹象表明，富含高脂肪和高糖的食物不仅会引发有害的生理状况，还会使控制认知和进食行为的大脑区域出现明显的结构改变。食物摄入加上神经元能量调节机制似乎构成了一个复杂的系统，以确保食物热量不超过身体需求。与此同时，诸如下丘脑（HTH）、海马体（HIP）和杏仁核（AMY）等边缘性进食中枢的致肥胖相关特性，倾向于通过不同神经肽的相互作用来控制饮食习惯。为此，我们旨在关联一种关键的抗肥胖神经肽受体即神经降压素1（NTR1）的表达差异与高脂饮食（HFD）处理的冬眠仓鼠（金黄地鼠）记忆表现之间的关系。有趣的是，这些仓鼠在处理的第5周从第12周体重显著增加（p < 0.01），同时伴有血脂胆固醇、甘油三酯和血糖水平升高。与此同时，这些仓鼠的自发活动减少，如探索行为、直立和梳理行为。更相关的是，它们在新物体识别（NOR）测试中识别新物体的能力极差（p < 0.001），并且没有正确选择条件性位置偏爱（CPP）装置中含有奖励的隔间。令人惊讶的是，HFD仓鼠行为和记忆任务的改变与上述边缘位点NTR1表达的变化密切相关，因此表明该神经元系统很可能是治疗肥胖相关记忆功能障碍的替代方案。
