Involvement of central cholinergic mechanisms on sodium intake induced by gabaergic activation of the lateral parabrachial nucleus

► Sodium satiety is disrupted by gabaergic activation in the LPBN. ► Central cholinergic mechanisms facilitate sodium intake to muscimol into the LPBN. ► Inhibition of central cholinergic mechanisms by LPBN is essential for sodium satiety. Bilateral injections of the GABAA agonist muscimol into the...

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Published in:	Neuroscience letters Vol. 534; pp. 188 - 192
Main Authors:	Asnar, Diego S., Roncari, Camila F., De Luca, Laurival A., de Paula, Patrícia M., Colombari, Débora S.A., Menani, José V.
Format:	Journal Article
Language:	English
Published:	Ireland Elsevier Ireland Ltd 08-02-2013
Subjects:	Angiotensin Receptor Antagonists - pharmacology Angiotensin-Converting Enzyme Inhibitors - pharmacology Animals Atropine - pharmacology Captopril - pharmacology Diuretics - pharmacology Drinking - drug effects Eating - drug effects Eating - physiology Furosemide - pharmacology GABA Agonists - pharmacology GABAA receptor Imidazoles - pharmacology Injections, Intraventricular Losartan - pharmacology Male Muscarinic Antagonists - pharmacology Muscarinic receptor Muscimol - pharmacology Pons - drug effects Pons - metabolism Rats Rats, Sprague-Dawley Receptors, GABA-A - metabolism Receptors, Muscarinic - metabolism Sodium appetite Sodium Chloride - metabolism Sodium satiety Thirst DOCA s.c CCK LV OVLT Sodium satiety NTS FURO ANG II CAP LPBN Sodium appetite CRF i.c.v Muscarinic receptor Thirst GABAA receptor SFO
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Summary:	► Sodium satiety is disrupted by gabaergic activation in the LPBN. ► Central cholinergic mechanisms facilitate sodium intake to muscimol into the LPBN. ► Inhibition of central cholinergic mechanisms by LPBN is essential for sodium satiety. Bilateral injections of the GABAA agonist muscimol into the lateral parabrachial nucleus (LPBN) disrupt satiety and induce strong ingestion of water and 0.3M NaCl in fluid-replete rats by mechanisms not completely clear. In the present study, we investigated the effects of the blockade of central muscarinic cholinergic receptors with atropine injected intracerebroventricularly (i.c.v.) on 0.3M NaCl and water intake induced by muscimol injections into the LPBN in fluid-replete rats. Male Holtzman rats with stainless steel cannulas implanted bilaterally into the LPBN and unilaterally into the lateral ventricle (LV) were used. Bilateral injections of muscimol (0.5nmol/0.2μL) into the LPBN induced 0.3M NaCl (32.2±9.9mL/4h, vs. saline: 0.4±0.2mL/4h) and water intake (11.4±4.4mL/4h, vs. saline: 0.8±0.4mL/4h) in fluid-replete rats previously treated with i.c.v. injection of saline. The previous i.c.v. injection of atropine (20nmol/1μL) reduced the effects of LPBN-muscimol on 0.3M NaCl (13.5±5.0mL/4h) and water intake (2.9±1.6mL/4h). The i.c.v. injection of atropine did not affect 0.3M NaCl (26.8±6.2mL/2h, vs. saline i.c.v.: 36.5±9.8mL/2h) or water intake (14.4±2.5mL/2h, vs. saline i.c.v.: 15.6±4.8mL/2h) in rats treated with furosemide+captopril subcutaneously combined with bilateral injections of moxonidine (α2-adrenoceptor/imidazoline agonist, 0.5nmol/0.2μL) into the LPBN, suggesting that the effect of atropine was not due to non-specific inhibition of ingestive behaviors. The results show that active central cholinergic mechanisms are necessary for the hypertonic NaCl and water intake induced by the blockade of the inhibitory mechanisms with injections of muscimol into the LPBN in fluid-replete rats. The suggestion is that in fluid-replete rats the action of LPBN mechanisms inhibits facilitatory signals produced by the activity of central cholinergic mechanisms to maintain satiety.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0304-3940 1872-7972
DOI:	10.1016/j.neulet.2012.11.042