Gabaergic and opioid receptors mediate the facilitation of NaCl intake induced by alfa 2-adrenergic activation in the lateral parabrachial nucleus.

Abstract

Alpha2-adrenergic, gabaergic or opioidergic activation in the lateral parabrachial nucleus (LPBN) increases sodium intake. In the present study, we investigated the effects of single or combined block-ade of opioidergic and gabaergic receptors in the LPBN on the increase of 0.3 M NaCl intake induced by _2-adrenoceptor activation in the LPBN. Male Holtzman rats (n = 5–9/group) with cannulas implanted bilaterally in the LPBN were treated with the diuretic furosemide (10 mg/kg b wt.) combined with low dose of the angiotensin converting enzyme inhibitor captopril (5 mg/kg b wt.) subcutaneously. Bilat-eral injections of moxonidine (alpha2-adrenergic/imidazoline receptor agonist, 0.5 nmol) into the LPBN increased furosemide + captopril-induced 0.3 M NaCl intake (25.8 ± 1.4, vs. vehicle: 3.8 ± 1.1 ml/60 min). The opioidergic receptor antagonist naloxone (100 nmol) or the GABAA receptor antagonist bicuculline (5 nmol) injected into the LPBN partially reduced the increase of 0.3 M NaCl intake produced by LPBN moxonidine (11.8 ± 4.0 and 22.8 ± 4.5, respectively, vs. vehicle + moxonidine: 31.6 ± 4.0 ml/60 min, respectively). Similar to the treatment with each antagonist alone, the combined injections of nalox-one (100 nmol) and bicuculline (5 nmol) into the LPBN also partially reduced moxonidine effects on 0.3 M NaCl intake (15.5 ± 6.5 ml/60 min). The GABAB receptor antagonist saclofen (5 nmol) injected into the LPBN did not change the effects of moxonidine on 0.3 M NaCl intake (24.3 ± 7.8 ml/120 min). These results suggest that the increase of 0.3 M NaCl intake by _2-adrenergic receptor activation in the LPBN is partially dependent on GABAA and opioid receptor activation in this area.