Participação do núcleo do trato solitário rostral e do núcleo parabraquial lateral no controle da ingestão de sódio

Abstract

The rostral portion of the nucleus of the solitary tract (rNTS), located in the medulla oblongata, is considered the first synaptic relay for integration of sodium taste sensorial information. The rNTS receives and send projections to different forebrain and hindbrain areas related to hydroeletrolitic balance control, including the lateral parabrachial nucleus (LPBN) in the pons. Separate activation of alpha2-adrenergic and P2 purinergic receptor, as well as GABAergic receptor activation, in LPBN facilitates hypertonic NaCl intake. Therefore, the aims of the present study were: a) to test if the inhibition of rNTS would change sodium-depletion induced sodium intake; b) to test if the LPBN GABAergic mechanism interfere with sodium palatability; and c) to investigate the effects of the blockage of purinergic receptors of the LPBN on the facilitation of 0.3 M NaCl intake induced by alpha2-adrenoceptor activation into the LPBN. Thus, male Wistar or Holtzman rats received bilateral LPBN or rNTS cannulas. In sodium-depleted (furosemide, 20 mg/kg b. wt. subcutaneously combined with sodium deficient diet for 24 h) male rats, bilateral injections of cobalt chloride (synaptic blocker, 1 mM/0.1 μl) caused a small increase (16.81.9 ml/60 min), while muscimol (GABAA receptor agonist, 120 pmol/0.1 μl) injections did not change sodium-depletion induced sodium intake (11.52.7 ml/60 min) in comparison to control treatment (11.11.4 ml/60 min). In satiated rats treated with muscimol (0.5 nmol/0.2 μl) injections into the LPBN, the number of hedonic (89 18) and aversive (2416) responses to intra-oral infusion of 0.3 M NaCl were not different from those observed after LPBN saline injections (11715 e 2310, respectively). Finally, in sodium-depleted rats bilateral LPBN injections of moxonidine (alpha2 adrenergic/imidalozine receptor agonist, 0.5 nmol/0.2 μl) into the LPBN increased sodium depletion-induced 0.3 M NaCl intake (29.27.6, vs. vehicle: 16.32.6 ml/120 min) and water intake (5.11.4, vs. vehicle: 1.60.8 ml/120 min). Pretreatment with suramim (non-selective P2 purinergic antagonist, 2 nmol/0.2 μl) abolished the effects of moxonidine on 0.3 M NaCl intake (14.06.9 ml/120 min) and water intake (1.60.5 ml/120 min). However, suramim alone into the LPBN almost abolished 0.3 NaCl intake (2.52.4 ml/120 min) and abolished water intake (0.10.1 ml/120 min) by sodium depleted rats. In another group of rats, bilateral injections of moxonidine (0.5 nmol/0.2 μl) into the LPBN increased sodium depletion-induced 0.3 M NaCl intake (29.7±4.2, vs. vehicle: 18.9±0.7 ml/120 min). The P2X purinergic antagonist PPADS (pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid, 4 nmol/0.2 μl) alone into the LPBN did not change 0.3 NaCl intake (18.5±4.6 ml/120 min).Therefore pretreatment with PPADS into the LPBN abolished the effects of moxonidine on 0.3 M NaCl intake (14.3±4.1 ml/120 min). In summary, present results suggest that a) synaptic blockade into rNTS might facilitate sodium intake; b) GABAergic mechanisms into the LPBN are not involved with sodium palatability in satiated ratsand c) α2-adrenergic and P2X purinergic receptors interact in the LPBN to facilitate sodium intake.