Mahía J, Bernal A, Puerto A
Psicobiología, Universidad de Granada, Campus de Cartuja, Granada, 18071, Spain.
Exp Brain Res. 2007 Oct;183(1):27-39. doi: 10.1007/s00221-007-1018-9. Epub 2007 Jul 14.
The aim of this study was to examine the dipsogenic mechanisms involved in the recently discovered tuberomammillary (TM)-mediated polydipsia. Rats with bilateral electrolytic lesions of each TM subnucleus underwent several dipsogenic treatments, both osmotic and volemic. Animals with ventral (E2) or medial TM lesions (E3 or E4) showed a potentiated hyperdipsic response to hypertonic sodium chloride administration but not to sucrose or polyethylene glycol treatments. The increase in response to sodium chloride was significantly greater in groups E3/E4 and E2 than in the non-lesioned group and in animals with polydipsia induced by lesion of the median eminence. As previously reported, hyperphagia was induced by lesion to ventral TM nuclei (E1 or E2), confirming a possible role for the TM complex in food intake. However, lesions in medial nuclei (E3 or E4) did not produce this increase in food intake. These results are interpreted in relation to the hypothalamic systems involved in food and water intake.
本研究的目的是探究参与最近发现的结节乳头体（TM）介导的烦渴的致渴机制。对每个TM亚核进行双侧电解损伤的大鼠接受了几种致渴处理，包括渗透性和容量性处理。腹侧（E2）或内侧TM损伤（E3或E4）的动物对高渗氯化钠给药表现出增强的高渗性烦渴反应，但对蔗糖或聚乙二醇处理无此反应。E3/E4组和E2组对氯化钠反应的增加显著大于未损伤组以及由正中隆起损伤诱导烦渴的动物。如先前报道，腹侧TM核（E1或E2）损伤可诱导多食，证实TM复合体在食物摄入中可能发挥作用。然而，内侧核（E3或E4）损伤并未导致食物摄入量增加。这些结果结合参与食物和水摄入的下丘脑系统进行了解释。
