Mechanisms involved in dual vasopressin/apelin neuron dysfunction during aging

Julie Sauvant, Jean-Christophe Delpech, Karine Palin, Nadia De Mota, Jennifer Dudit, Agnès Aubert, Hélène Orcel, Pascale Roux, Sophie Layé, Françoise Moos, Catherine Llorens-Cortes, Agnès Nadjar
PLoS ONE. 2014-02-05; 9(2): e87421
DOI: 10.1371/journal.pone.0087421

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1. PLoS One. 2014 Feb 5;9(2):e87421. doi: 10.1371/journal.pone.0087421. eCollection
2014.

Mechanisms involved in dual vasopressin/apelin neuron dysfunction during aging.

Sauvant J(1), Delpech JC(1), Palin K(1), De Mota N(2), Dudit J(1), Aubert A(1),
Orcel H(3), Roux P(1), Layé S(1), Moos F(1), Llorens-Cortes C(2), Nadjar A(1).

Author information:
(1)Nutrition et Neurobiologie Intégrée, UMR 1286, INRA, Bordeaux, France ;
Nutrition et Neurobiologie Intégrée, UMR 1286, Univ. Bordeaux, Bordeaux, France.
(2)Center for Interdisciplinary Research in Biology (CIRB), U1050, INSERM,
Collège de France, Université Pierre et Marie Curie-Paris VI, Paris, France.
(3)Institut de GénomiqueFonctionnelle, PharmacologieMoléculaire, UMR 5203, CNRS,
Montpellier, France.

Normal aging is associated with vasopressin neuron adaptation, but little is
known about its effects on the release of apelin, an aquaretic peptide
colocalized with vasopressin. We found that plasma vasopressin concentrations
were higher and plasma apelin concentrations lower in aged rats than in younger
adults. The response of AVP/apelin neurons to osmotic challenge was impaired in
aged rats. The overactivity of vasopressin neurons was sustained partly by the
increased expression of Transient receptor potential vanilloid2 (Trpv2), because
central Trpv blocker injection reversed the age-induced increase in plasma
vasopressin concentration without modifying plasma apelin concentration. The
morphofunctional plasticity of the supraoptic nucleus neuron-astrocyte network
normally observed during chronic dehydration in adults appeared to be impaired in
aged rats as well. IL-6 overproduction by astrocytes and low-grade microglial
neuroinflammation may contribute to the modification of neuronal functioning
during aging. Indeed, central treatment with antibodies against IL-6 decreased
plasma vasopressin levels and increased plasma apelin concentration toward the
values observed in younger adults. Conversely, minocycline treatment (inhibiting
microglial metabolism) did not affect plasma vasopressin concentration, but
increased plasma apelin concentration toward control values for younger adults.
This study is the first to demonstrate dual vasopressin/apelin adaptation
mediated by inflammatory molecules and neuronal Trpv2, during aging.

DOI: 10.1371/journal.pone.0087421
PMCID: PMC3914823
PMID: 24505289 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus