Department of Physiology and Pathology, São Paulo State University, UNESP, Araraquara, SP, Brazil.
Brain Res. 2011 Feb 4;1372:49-58. doi: 10.1016/j.brainres.2010.11.075. Epub 2010 Dec 1.
Purinergic receptors are present in the lateral parabrachial nucleus (LPBN), a pontine structure involved in the control of sodium intake. In the present study, we investigated the effects of α,β-methyleneadenosine 5'-triphosphate (α,β-methylene ATP, selective P2X purinergic agonist) alone or combined with pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, P2X purinergic antagonist) or suramin (non-selective P2 purinergic antagonist) injected into the LPBN on sodium depletion-induced 1.8% NaCl intake. Male Holtzman rats with stainless steel cannulas implanted into the LPBN were used. Sodium depletion was induced by treating rats with the diuretic furosemide (20mg/kg of body weight) followed by 24h of sodium-deficient diet. Bilateral injections of α,β-methylene ATP (2.0 and 4.0nmol/0.2μl) into the LPBN increased sodium depletion-induced 1.8% NaCl intake (25.3±0.8 and 26.5±0.9ml/120min, respectively, vs. saline: 15.2±1.3ml/120min). PPADS (4nmol/0.2μl) alone into the LPBN did not change 1.8% NaCl intake, however, pretreatment with PPADS into the LPBN abolished the effects of α,β-methylene ATP on 1.8% NaCl intake (16.9±0.9ml/120min). Suramin (2.0nmol/0.2μl) alone into the LPBN reduced sodium depletion-induced 1.8% NaCl intake (5.7±1.9ml/120min, vs. saline: 15.5±1.1ml/120min), without changing 2% sucrose intake or 24h water deprivation-induced water intake. The combination of suramin and α,β-methylene ATP into the LPBN produced no change of 1.8% NaCl intake (15.2±1.2ml/120min). The results suggest that purinergic P2 receptor activation in the LPBN facilitates NaCl intake, probably by restraining LPBN mechanisms that inhibit sodium intake.
嘌呤能受体存在于外侧臂旁核（LPBN）中，这是一种参与控制钠摄入的桥脑结构。在本研究中，我们研究了单独使用α，β-亚甲基腺苷 5'-三磷酸（α，β-亚甲基 ATP，选择性 P2X 嘌呤能激动剂）或与吡啶醛 6-偶氮苯-2'，4'-二磺酸（PPADS，P2X 嘌呤能拮抗剂）或苏拉明（非选择性 P2 嘌呤能拮抗剂）联合注射到 LPBN 对钠耗竭诱导的 1.8%NaCl 摄入的影响。使用植入 LPBN 不锈钢套管的雄性霍尔茨曼大鼠进行了实验。通过用利尿剂呋塞米（20mg/kg 体重）处理大鼠来诱导钠耗竭，随后进行 24 小时的低钠饮食。双侧 LPBN 注射α，β-亚甲基 ATP（2.0 和 4.0nmol/0.2μl）增加了钠耗竭诱导的 1.8%NaCl 摄入（分别为 25.3±0.8 和 26.5±0.9ml/120min，而生理盐水为 15.2±1.3ml/120min）。单独向 LPBN 中注射 PPADS（4nmol/0.2μl）不会改变 1.8%NaCl 摄入，但预先向 LPBN 中注射 PPADS 可消除α，β-亚甲基 ATP 对 1.8%NaCl 摄入的影响（16.9±0.9ml/120min）。单独向 LPBN 中注射苏拉明（2.0nmol/0.2μl）降低了钠耗竭诱导的 1.8%NaCl 摄入（5.7±1.9ml/120min，而生理盐水为 15.5±1.1ml/120min），但不改变 2%蔗糖摄入或 24 小时禁水诱导的水摄入。向 LPBN 中联合注射苏拉明和α，β-亚甲基 ATP 不会改变 1.8%NaCl 摄入（15.2±1.2ml/120min）。结果表明，LPBN 中的嘌呤能 P2 受体激活促进了 NaCl 摄入，这可能是通过抑制 LPBN 抑制钠摄入的机制来实现的。
