大鼠臂旁核损伤会破坏速尿诱导的钠食欲，但不会破坏钙缺乏诱导的钠食欲。
Parabrachial lesions in rats disrupt sodium appetite induced by furosemide but not by calcium deprivation.
作者信息
Grigson P S, Colechio E M, Power M L, Schulkin J, Norgren R
机构信息
Department of Neural and Behavioral Sciences, College of Medicine, The Pennsylvania State University, 500 University Drive, Hershey, PA 17033, USA.
Nutrition Laboratory and Conservation Ecology Center, Smithsonian Conservation Biology Institute, National Zoological Park, P. O. Box 37012, MRC 5503, Washington, DC 20013-7012, USA.
出版信息
Physiol Behav. 2015 Mar 1;140:172-9. doi: 10.1016/j.physbeh.2014.11.070. Epub 2014 Dec 22.
An appetite for CaCl2 and NaCl occurs in young rats after they are fed a diet lacking Ca or Na, respectively. Bilateral lesions of the parabrachial nuclei (PBN) disrupt normal taste aversion learning and essentially eliminate the expression of sodium appetite. Here we tested whether similar lesions of the PBN would disrupt the calcium-deprivation-induced appetite for CaCl2 or NaCl. Controls and rats with PBN lesions failed to exhibit a calcium-deprivation-induced appetite for CaCl2. Nevertheless, both groups did exhibit a significant calcium-deprivation-induced appetite for 0.5M NaCl. Thus, while damage to the second central gustatory relay in the PBN disrupts the appetite for 0.5M NaCl induced by furosemide, deoxycorticosterone acetate, and polyethylene glycol, the sodium appetite induced by dietary CaCl2 depletion remains intact.
分别给幼鼠喂食缺钙或缺钠的饮食后，它们会出现对氯化钙和氯化钠的食欲。臂旁核（PBN）的双侧损伤会破坏正常的味觉厌恶学习，并基本消除钠食欲的表现。在这里，我们测试了PBN的类似损伤是否会破坏钙缺乏诱导的对氯化钙或氯化钠的食欲。对照组和PBN损伤的大鼠均未表现出钙缺乏诱导的对氯化钙的食欲。然而，两组均表现出显著的钙缺乏诱导的对0.5M氯化钠的食欲。因此，虽然PBN中第二级中枢味觉中继受损会破坏速尿、醋酸脱氧皮质酮和聚乙二醇诱导的对0.5M氯化钠的食欲，但饮食中氯化钙缺乏诱导的钠食欲仍然完好无损。
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