Research ReportPurinergic mechanisms of lateral parabrachial nucleus facilitate sodium depletion-induced NaCl intake

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 (20 mg/kg of body weight) followed by 24 h of sodium-deficient diet. Bilateral injections of α,β-methylene ATP (2.0 and 4.0 nmol/0.2 μl) into the LPBN increased sodium depletion-induced 1.8% NaCl intake (25.3 ± 0.8 and 26.5 ± 0.9 ml/120 min, respectively, vs. saline: 15.2 ± 1.3 ml/120 min). PPADS (4 nmol/0.2 μl) 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 ± 0.9 ml/120 min). Suramin (2.0 nmol/0.2 μl) alone into the LPBN reduced sodium depletion-induced 1.8% NaCl intake (5.7 ± 1.9 ml/120 min, vs. saline: 15.5 ± 1.1 ml/120 min), without changing 2% sucrose intake or 24 h 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 ± 1.2 ml/120 min). The results suggest that purinergic P2 receptor activation in the LPBN facilitates NaCl intake, probably by restraining LPBN mechanisms that inhibit sodium intake.

Research highlights► Purinergic P2 receptor blockade in the LPBN did not affect water or sucrose intake. ► P2 receptors are involved in the LPBN inhibitory mechanisms for sodium intake.