Lateral parabrachial nucleus and opioid mechanisms of the central nucleus of the amygdala in the control of sodium intake

Abstract

Facilitatory and inhibitory mechanisms in the central nucleus of the amygdala (CeA) and the lateral parabrachial nucleus (LPBN), respectively, are important for the control of sodium and water intake. Here we investigated the importance of the opioid mechanisms in the CeA for water and 0.3 M NaCl intake in euhydrated or hyperosmotic rats treated with injections of muscimol (GABAA agonist) or moxonidine (α2 adrenergic/imidazoline agonist) into the LPBN, respectively. Male Holtzman rats (n = 4–8/group) with stainless steel cannulas implanted bilaterally in the CeA and in the LPBN were used. The ingestion of 0.3 M NaCl and water by euhydrated rats treated with muscimol (0.5 nmol/0.2 μl) into the LPBN (29.4 ± 2.7 and 15.0 ± 2.4 ml/4 h, respectively) was abolished by the previous injections of naloxone (opioid antagonist, 40 μg/0.2 μl) into the CeA (0.7 ± 0.3 and 0.3 ± 0.1 ml/4 h, respectively). The ingestion of 0.3 M NaCl by rats treated with intragastric 2 M NaCl (2 ml/rat) combined with moxonidine (0.5 nmol/0.2 μl) into the LPBN (17.0 ± 3.8 ml/2 h) was also strongly reduced by the previous injections of naloxone into the CeA (3.2 ± 2.5 ml/2 h). Sucrose intake was not affected by naloxone injections into the CeA, which minimized the possibility of non-specific inhibition of ingestive behaviors with this treatment. The present results suggest that opioid mechanisms in the CeA are essential for hypertonic NaCl intake when the LPBN inhibitory mechanisms are deactivated or attenuated with injections of muscimol or moxonidine in this area.