Watson P J, Biderman M D, Warfield D R
Int J Neurosci. 1981;15(1-2):95-8. doi: 10.3109/00207458108985848.
Neurologically intact rats were presented with a 0.2% (w/v) quinine adulterated water supply, and they failed to meter fluid consumption homeostatically in accordance with the elevated food intake that followed glucoprivation induced by 250, 500, and 750 mg/kg injections of 2-deoxy-D-glucose (2DG). These animals, nevertheless, were statistically indistinguishable from controls in the amount of food eaten following the 2DG treatments. These data suggest that the hypodipsia produced by some brain lesions is not a sufficient stimulus to produce the deficient glucoprivic feeding that accompanies such lesions; therefore, future lesion investigations that simultaneously yield hypodipsia and reduced eating in response to 2DG need not employ hypodipsic neurologically intact controls.
给神经功能正常的大鼠提供含有0.2%（w/v）奎宁的掺假水源，它们无法根据250、500和750mg/kg注射2-脱氧-D-葡萄糖（2DG）诱导的糖剥夺后增加的食物摄入量，以稳态方式调节液体消耗。然而，在2DG处理后，这些动物的食物摄入量与对照组在统计学上没有差异。这些数据表明，某些脑损伤产生的饮水减少并不是产生伴随此类损伤的糖剥夺性摄食不足的充分刺激；因此，未来同时产生饮水减少和对2DG反应性进食减少的损伤研究不必采用饮水减少的神经功能正常的对照。
