Hu B, Qiao H, Sun B, Jia R, Fan Y, Wang N, Lu B, Yan J Q
Department of Physiology and Pathophysiology, Xi'an Jiaotong University, Health Science Center, 76# West Yanta Road, Xi'an, Shaanxi 710061, PR China; Department of Prosthodontics, Xi'an Jiaotong University, College of Stomatology, 98# Xiwu Road, Xi'an, Shaanxi 710004, PR China.
Department of Physiology and Pathophysiology, Xi'an Jiaotong University, Health Science Center, 76# West Yanta Road, Xi'an, Shaanxi 710061, PR China.
Neuroscience. 2015 Oct 29;307:302-10. doi: 10.1016/j.neuroscience.2015.08.069. Epub 2015 Sep 3.
The blockade of the central nucleus of the amygdala (CeA) with the GABAA receptor agonist muscimol significantly reduces hypertonic NaCl and water intake by sodium-depleted rats. In the present study we investigated the effects of previous injection of losartan, an angiotensin II type-1 (AT1) receptor antagonist, into the CeA on 0.3M NaCl and water intake reduced by muscimol bilaterally injected into the same areas in rats submitted to water deprivation-partial rehydration (WD-PR) and in rats treated with the diuretic furosemide (FURO). Male Sprague-Dawley rats with stainless steel cannulas bilaterally implanted into the CeA were used. Bilateral injections of muscimol (0.2 nmol/0.5 μl, n=8 rats/group) into the CeA in WD-PR-treated rats reduced 0.3M NaCl intake and water intake, and pre-treatment of the CeA with losartan (50 μg/0.5 μl) reversed the inhibitory effect of muscimol. The negative effect of muscimol on sodium and water intake could also be blocked by pretreatment with losartan microinjected into the CeA in rats given FURO (n=8 rats/group). However, bilateral injections of losartan (50 μg/0.5 μl) alone into the CeA did not affect the NaCl or water intake. These results suggest that the deactivation of CeA facilitatory mechanisms by muscimol injection into the CeA is promoted by endogenous angiotensin II acting on AT1 receptors in the CeA, which prevents rats from ingesting large amounts of hypertonic NaCl and water.
用GABAA受体激动剂蝇蕈醇阻断杏仁核中央核（CeA）可显著减少缺钠大鼠的高渗氯化钠摄入和水摄入。在本研究中，我们调查了预先向CeA注射血管紧张素II 1型（AT1）受体拮抗剂氯沙坦，对经水剥夺-部分补液（WD-PR）处理的大鼠以及用利尿剂呋塞米（FURO）处理的大鼠，双侧注射蝇蕈醇至同一区域后0.3M氯化钠和水摄入的影响。使用双侧植入CeA不锈钢套管的雄性Sprague-Dawley大鼠。在WD-PR处理的大鼠中，双侧向CeA注射蝇蕈醇（0.2 nmol/0.5 μl，每组8只大鼠）可减少0.3M氯化钠摄入和水摄入，而用氯沙坦（50 μg/0.5 μl）预处理CeA可逆转蝇蕈醇的抑制作用。在给予FURO的大鼠中，预先向CeA微量注射氯沙坦也可阻断蝇蕈醇对钠和水摄入的负面影响（每组8只大鼠）。然而，单独双侧向CeA注射氯沙坦（50 μg/0.5 μl）并不影响氯化钠或水的摄入。这些结果表明，向CeA注射蝇蕈醇使CeA促进机制失活，这是由内源性血管紧张素II作用于CeA中的AT1受体所促进的，从而阻止大鼠摄入大量高渗氯化钠和水。
