Research ReportImportance of the central nucleus of the amygdala on sodium intake caused by deactivation of lateral parabrachial nucleus

- Sodium satiety is controlled by central amygdala and lateral parabrachial nucleus.
- Sodium intake to lateral parabrachial deactivation depends on central amygdala.
- Facilitation sodium intake by central amygdala is inhibited by parabrachial nucleus.
- Deactivation of the lateral parabrachial nucleus disrupts sodium satiety.
- CeA facilitatory and LPBN inhibitory mechanisms interacts to control of NaCl intake.

The lateral parabrachial nucleus (LPBN) and the central nucleus of the amygdala (CeA) are important central areas for the control of sodium appetite. In the present study, we investigated the importance of the facilitatory mechanisms of the CeA on NaCl and water intake produced by the deactivation of LPBN inhibitory mechanisms. Male Holtzman rats (n=7-14) with stainless steel cannulas implanted bilaterally in the CeA and LPBN were used. Bilateral injections of moxonidine (α2-adrenoceptor/imidazoline agonist, 0.5 nmol/0.2 μl) into the LPBN increased furosemide+captopril-induced 0.3 M NaCl (29.7±7.2, vs. vehicle: 4.4±1.6 ml/2 h) and water intake (26.4±6.7, vs. vehicle: 8.2±1.6 ml/2 h). The GABAA agonist muscimol (0.25 nmol/0.2 μl) injected bilaterally into the CeA abolished the effects of moxonidine into the LPBN on 0.3 M NaCl (2.8±1.6 ml/2 h) and water intake (3.3±2.3 ml/2 h). Euhydrated rats treated with muscimol (0.5 nmol/0.2 μl) into the LPBN also ingested 0.3 M NaCl (19.1±6.4 ml/4 h) and water (8.8±3.2 ml/4 h). Muscimol (0.5 nmol/0.2 μl) into the CeA also abolished 0.3 M NaCl (0.1±0.04 ml/4 h) and water intake (0.1±0.02 ml/4 h) in euhydrated treated with muscimol into the LPBN. The present results show that neuronal deactivation of the CeA abolishes NaCl intake produced by the blockade of LPBN inhibitory mechanisms, suggesting an interaction between facilitatory mechanisms of the CeA and inhibitory mechanisms of the LPBN in the control of NaCl intake.