Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, Xi'an Jiaotong University College of Stomatology, 98# Xiwu Road, Xi'an, Shaanxi, 710061, PR China; Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Science, 76# W. Yanta Road, Xi'an, Shaanxi, 710061, PR China.
Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Science, 76# W. Yanta Road, Xi'an, Shaanxi, 710061, PR China.
Brain Res Bull. 2018 Oct;143:132-137. doi: 10.1016/j.brainresbull.2018.08.018. Epub 2018 Aug 28.
The central nucleus of the amygdala (CeA) is a critical region in regulating sodium intake, and interestingly, purinergic receptors reportedly related to fluid balance, are also expressed in CeA. In this study, we investigated whether the purinergic mechanisms of CeA were involved in regulating sodium intake. Male Sprague-Dawley rats had cannulas implanted bilaterally into the CeA and were sodium depleted with furosemide (FURO 20 mg/kg) plus 24 h-sodium deficient food fed. Bilateral injections of the P2X purinergic agonist, α,β-methyleneadenosine 5'-triphosphate (α,β-methylene ATP 1.0, 2.0, 4.0 nmol, respectively) into the CeA region induced dose-related reductions in sodium intake without affecting water intake. Injection of P2X purinergic antagonist, pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS 4.0 nmol/0.5 μl) into the CeA region did not alter sodium and water intake, however, prior injection of PPADS into the CeA area abolished the inhibitory effects on sodium intake by α,β-methylene ATP. Interestingly, prior injection of γ-aminobutyric acid type A (GABA) receptor antagonist, bicuculline (4.0 nmol/0.5 μl) into the CeA region partially reversed the deficit of sodium intake induced by α,β-methylene ATP. These results suggest that purinergic receptors in the CeA are involved in the control of sodium intake in the sodium-depleted rats and this negative modulation may be, at least partly, mediated by the GABA receptor.
杏仁中央核（CeA）是调节钠摄入的关键区域，有趣的是，据报道与液体平衡有关的嘌呤能受体也在 CeA 中表达。在这项研究中，我们研究了 CeA 中的嘌呤能机制是否参与调节钠摄入。雄性 Sprague-Dawley 大鼠双侧植入 CeA 套管，并给予呋塞米（FURO 20mg/kg）加 24 小时钠缺乏食物喂养以耗尽钠。将 P2X 嘌呤能激动剂 α,β-亚甲基腺苷 5'-三磷酸（α,β-亚甲基 ATP，分别为 1.0、2.0、4.0nmol）双侧注射到 CeA 区域，可引起剂量相关的钠摄入减少，而不影响水摄入。将 P2X 嘌呤能拮抗剂吡哆醛-6-偶氮苯-2',4'-二磺酸（PPADS，4.0nmol/0.5μl）注射到 CeA 区域不会改变钠和水的摄入，但预先将 PPADS 注射到 CeA 区域可消除 α,β-亚甲基 ATP 对钠摄入的抑制作用。有趣的是，预先将 GABA 受体拮抗剂荷包牡丹碱（bicuculline，4.0nmol/0.5μl）注射到 CeA 区域可部分逆转由 α,β-亚甲基 ATP 引起的钠摄入不足。这些结果表明，CeA 中的嘌呤能受体参与了钠耗竭大鼠的钠摄入控制，这种负向调节至少部分是由 GABA 受体介导的。
