Lorden J, Oltmans G A, Margules D L
J Comp Physiol Psychol. 1976 Feb;90(2):144-55. doi: 10.1037/h0077201.
The ventral noradrenergic bundle (VB) of the rate brain has been proposed as the substrate for the hyperphagia and obesity produced by ventromedial hypothalamic lesions. To determine the relationship between body weight and damage to the VB, the effects of bilateral electrolytic and 6-hydroxy-dopamine (6-OHDA) lesions of the VB were compared. When rats were fed only a standard laboratory diet, no significant differences were found between groups. When a high-fat diet supplement was introduced, the group with electrolytic lesions became significantly heavier than the control group; however, the 6-OHDA group did not differ from the controls. Norepinephrine depletion was significantly greater following the 6-OHDA than the electrolytic lesions. Both lesions reduced telencephalic dopamine and serotonin only slightly. A second study in which both types of lesions were placed at a rostral ventromedial hypothalamic site yielded the same pattern of results. Diet-dependent increases in body weight were attributed to the destruction of a non-noradrenergic system, which was spared by the relatively selective 6-OHDA lesion but damaged by the nonselective electrolytic lesion.
延髓腹侧去甲肾上腺素能束(VB)被认为是腹内侧下丘脑损伤所致食欲亢进和肥胖的基础。为了确定体重与VB损伤之间的关系,比较了VB双侧电解损伤和6-羟基多巴胺(6-OHDA)损伤的效果。当大鼠仅喂食标准实验室饮食时,各实验组之间未发现显著差异。当引入高脂肪饮食补充剂时,电解损伤组的体重显著高于对照组;然而,6-OHDA组与对照组无差异。6-OHDA损伤后去甲肾上腺素的耗竭显著大于电解损伤。两种损伤均仅轻微降低端脑多巴胺和5-羟色胺。第二项研究将两种损伤均置于延髓腹内侧下丘脑前部,得到了相同的结果模式。饮食依赖性体重增加归因于一个非去甲肾上腺素能系统的破坏,该系统在相对选择性的6-OHDA损伤中未受影响,但在非选择性的电解损伤中受损。