Non-NMDA receptors in the lateral parabrachial nucleus modulate sodium appetite

Glutamatergic mechanisms have been implicated in the control of fluid ingestion. In the present study, we investigated whether non-N-methyl-d-aspartate (NMDA) glutamatergic receptors in the lateral parabrachial nucleus (LPBN) are involved in the control of water and sodium intake. Male Sprague–Dawley rats had cannulas implanted bilaterally into the LPBN. They were acutely depleted of water and sodium by injections of the diuretic furosemide (Furo; 10 mg/kg, bw) and given a low dose of the angiotensin-converting enzyme inhibitor, captopril (Cap; 5 mg/kg, bw). Bilateral LPBN injections of the non-NMDA receptor antagonist DNQX (2 and 5 nmol/0.2 μl) increased the ingestion of 0.3 M NaCl and water of Furo/Cap treated rats. The increased ingestion produced by DNQX was abolished by pretreating the LPBN with α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), a non-NMDA receptor agonist. AMPA injected alone into the LPBN reduced water and 0.3 M NaCl intake. Injections of DNQX (5 nmol/0.2 μl) into the LPBN also produced ingestion of 0.3 M NaCl after sc injections of the β-adrenoceptor agonist, isoproterenol, a hypotensive drug that typically produces only water intake. Food intake, arterial blood pressure and heart rate were not altered by DNQX LPBN injections. We conclude that agonists acting on non-NMDA receptors in the LPBN exert an inhibitory influence on sodium intake during acute fluid depletion with hypotension and after isoproterenol treatment. A possible interaction of serotonin with glutamate within the LPBN is discussed.