Luz Carla, Souza Anderson, Reis Rodolfo, Fregoneze Josmara Bartolomei, de Castro e Silva Emilio
Department of Biological Sciences, State University of Southwest Bahia, Jequié, Brazil.
Brain Res. 2006 Jul 12;1099(1):121-32. doi: 10.1016/j.brainres.2006.04.083. Epub 2006 Jun 12.
In the present study, we investigated the role of 5-HT(3) and 5-HT(2C) receptors located within the medial amygdala (MeA) in the control of water and salt intake in sodium-depleted rats. Pharmacological activation of 5-HT(3) receptors located in the medial amygdala by the selective 5-HT(3) receptor agonist m-CPBG significantly reduced salt intake in sodium-depleted rats, an effect that is reverted by pretreatment with the selective 5-HT(3) receptor antagonist ondansetron. In addition, the injection of ondansetron alone into the medial amygdala had no effect on salt intake in sodium-depleted and in sodium-repleted rats. Pharmacological stimulation of 5-HT(2C) receptors located in the medial amygdala by the selective 5-HT(2C) receptor agonist m-CPP failed to modify salt intake in sodium-depleted rats, whereas the blockade of these receptors by the selective 5-HT(2C) receptor antagonist SDZ SER 082 significantly reduced salt intake in this same group of animals. These results lead to the conclusion that the pharmacological activation of 5-HT(3) receptors located within the MeA inhibits salt intake in sodium-depleted rats and that, in this same brain region, the functional integrity of 5-HT(2C) receptors is required to achieve the full expression of sodium appetite in sodium-depleted rats.
在本研究中，我们调查了位于内侧杏仁核（MeA）的5-羟色胺（5-HT）3型和5-HT2C型受体在缺钠大鼠水盐摄入控制中的作用。选择性5-HT3型受体激动剂间氯苯甲酰胍（m-CPBG）对位于内侧杏仁核的5-HT3型受体进行药理激活，可显著降低缺钠大鼠的盐摄入量，而用选择性5-HT3型受体拮抗剂昂丹司琼预处理可逆转这一效应。此外，单独向内侧杏仁核注射昂丹司琼对缺钠和钠充足大鼠的盐摄入量均无影响。选择性5-HT2C型受体激动剂m-CPP对位于内侧杏仁核的5-HT2C型受体进行药理刺激，未能改变缺钠大鼠的盐摄入量，而选择性5-HT2C型受体拮抗剂SDZ SER 082对这些受体的阻断则显著降低了同一组动物的盐摄入量。这些结果得出如下结论：位于MeA的5-HT3型受体的药理激活可抑制缺钠大鼠的盐摄入量，并且在同一脑区，5-HT2C型受体的功能完整性是缺钠大鼠充分表达钠食欲所必需的。
