Gabaergic and opioid receptors mediate the facilitation of NaCl intake induced by α2-adrenergic activation in the lateral parabrachial nucleus

• Published in: Behavioural brain research Vol. 278; pp. 535 - 541
• Main Authors: Andrade, C.A.F., De Oliveira, L.B., Andrade-Franzé, G.M.F., De Luca Jr, L.A., Colombari, Débora S.A., Menani, J.V.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.02.2015
• Subjects: Adrenergic; Animals; Antihypertensive Agents - pharmacology; Baclofen - pharmacology; Bicuculline - pharmacology; Captopril - pharmacology; Dehydration; Enzyme Inhibitors - pharmacology; Furosemide - pharmacology; GABA; GABA-A Receptor Antagonists - pharmacology; GABA-B Receptor Agonists - pharmacology; Imidazoles - pharmacology; Male; Naloxone - pharmacology; Narcotic Antagonists - pharmacology; Opioid; Parabrachial Nucleus - drug effects; Parabrachial Nucleus - metabolism; Rats; Rats, Sprague-Dawley; Receptors, Adrenergic, alpha-2 - metabolism; Receptors, GABA - metabolism; Receptors, Opioid - metabolism; Sodium appetite; Sodium Chloride - metabolism; Sodium Potassium Chloride Symporter Inhibitors - pharmacology; Thirst; GABA; Opioid; Adrenergic; Sodium appetite; Dehydration; Thirst
• ISSN: 0166-4328; 1872-7549
• DOI: 10.1016/j.bbr.2014.10.007

•α2-adrenoceptor activation in the LPBN increases sodium intake in fluid-depleted rat.•Opioidergic receptor blockade partially reduced α2-adrenoceptor activation effects.•α2-adrenoceptor activation effects are partially reduced by GABAA receptor blockade.•Opioidergic/GABAergic blockade partially reduced α2-adrenoceptor activation effects.•α2-adrenoceptor activation effects are partially dependent on opioid/GABAA receptors. 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 blockade of opioidergic and gabaergic receptors in the LPBN on the increase of 0.3M NaCl intake induced by α2-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 (10mg/kgbwt.) combined with low dose of the angiotensin converting enzyme inhibitor captopril (5mg/kgbwt.) subcutaneously. Bilateral injections of moxonidine (alpha2-adrenergic/imidazoline receptor agonist, 0.5nmol) into the LPBN increased furosemide+captopril-induced 0.3M NaCl intake (25.8±1.4, vs. vehicle: 3.8±1.1ml/60min). The opioidergic receptor antagonist naloxone (100nmol) or the GABAA receptor antagonist bicuculline (5nmol) injected into the LPBN partially reduced the increase of 0.3M NaCl intake produced by LPBN moxonidine (11.8±4.0 and 22.8±4.5, respectively, vs. vehicle+moxonidine: 31.6±4.0ml/60min, respectively). Similar to the treatment with each antagonist alone, the combined injections of naloxone (100nmol) and bicuculline (5nmol) into the LPBN also partially reduced moxonidine effects on 0.3M NaCl intake (15.5±6.5ml/60min). The GABAB receptor antagonist saclofen (5nmol) injected into the LPBN did not change the effects of moxonidine on 0.3M NaCl intake (24.3±7.8ml/120min). These results suggest that the increase of 0.3M NaCl intake by α2-adrenergic receptor activation in the LPBN is partially dependent on GABAA and opioid receptor activation in this area.