title: Acute sodium depletion modifies septo-preoptic neuron sensitivities to neurohormones.
abstract: Sodium (Na+) depletion induces sodium appetite to replenish Na+ loss. It appears to be a consequence of enhanced levels of aldosterone (Aldo) and angiotensin II (AII) in the plasma as well as in the brain. Mineralocorticoid pretreatment modifies the sensitivity of septo-preoptic neurons to locally applied AII and Aldo. Therefore, we investigated septo-preoptic neuronal sensitivities to AII and Aldo, as well as to the specific AII type-1 receptor (AT-1) non-peptide antagonist losartan (Los) and to the specific AII type-2 receptor (AT-2) non-peptide antagonist PD123319 after one Na+ depletion without repletion. We found that one Na+ depletion induced increases in the proportion of neurons inhibited by iontophoretic application of AII (20.5% vs. 7.8%, p=0.004) whereas, the proportion of neurons excited by Aldo was increased, (23.7% vs. 5%, p=0.001). Moreover, the proportion of neurons changing sensitivity to AII after one application of Aldo was increased in the furosemide group (44.2% vs. 20.4%, p=0.0123). The proportion of neurons inhibited by application of losartan was enhanced, (26.4% vs. 9.3%, p=0.03). No significant changes were found in response to PD123319 by itself. Moreover, there were more neurons which co-localized responses to both Los and PD123319 in the furosemide group than in the control group (29.7% vs. 8.6%, p=0.027). It is known that multidepletions induce an increased need-free sodium appetite and our present findings could well form part of the neuronal basis of this behavior.
authors.affiliation: CNRS UPR 9054 Groupe de Neurobiologie des Régulations, I.E.S.G.C.A., Campus de l'Université de Bourgogne, 15 rue Hugues Picardet, 21000 Dijon, France.
authors.forename: F
authors.initials: F
authors.lastname: Liénard
authors.forename: O
authors.initials: O
authors.lastname: Galaverna
authors.forename: S N
authors.initials: SN
authors.lastname: Thornton
authors.forename: M J
authors.initials: MJ
authors.lastname: Meile
authors.forename: S
authors.initials: S
authors.lastname: Nicolaïdis
mesh_terms: D000450:Aldosterone / Q000494:pharmacology*; D000804:Angiotensin II / Q000494:pharmacology*; D000809:Angiotensins; D000818:Animals; D007093:Imidazoles / Q000494:pharmacology; D019808:Losartan / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D011301:Preoptic Area / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D011725:Pyridines / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012688:Septum Pellucidum / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*
chemical_list: D000809:Angiotensins; D007093:Imidazoles; D011725:Pyridines; D000804:Angiotensin II; C073402:PD 123319; D000450:Aldosterone; D012964:Sodium; D019808:Losartan