Acute ghrelin effects on memory retention in an olfactory bulbectomy model: a possible mechanism of action

MARIA BELEN PORETTI; SANTIAGO BIACONI; GIULIA MAESTRI; PAULA RODRIGUEZ; SUSANA RUBIALES DE BARIOGLIO; HELGI B. SCHIOTH; VALERIA PAOLA CARLINI

Mar del Plata

Congreso; LXI Reunión Científica Anual de la Sociedad Argentina de Investigación Clínica (SAIC)/ LXIV Reunión Anual de la Sociedad Argentina de Inmunología (SAI)/ XLVII Reunión Anual de la Sociedad Argentina de Farmacología Experimental.; 2016

SAIC, SAI, SAFE

Ghrelin (Ghr) is an orexigenic peptide that is being investigated for its potential role in development of anxiety-like behavior and modulation of depressive-like symptoms induced by bilateral olfactory bulbectomy (OB) in rodents. Olfactory bulbectomy is a useful animal model to study of depression and Ghr could be an alternative therapeutic tool in depression therapy. In present work, we studied the ability of Ghr to reverse amnesic effects induced by OB in mice, using the object recognition test (ORT) and possible Ghr effects on genes implicated in memory modulation into hippocampus. Adult male Albino Swiss mice were divided in sham and OB, and immediately after training in ORT were infused with saline (S) or Ghr 0.03 nmol/µl (doses that reversed depressive-like behavior induced by OB in tail suspension test) in the hippocampus. Animals were tested in ORT, sacrificed and hippocampus was dissected in order to study the mRNA expression of genes related to memory using real time PCR.The OB animals treated with S (OB-S) presented impair on memory retention compared to sham (p<0.05), but acute Ghr 0.03 nmol/µl infusion produced an increase on this parameter in OB animals (p ≤0.05). In addition, OB induced low expression of Calcium/calmodulin-dependent protein kinase II isoform2 (CamKII iso2) (F= 9.12, p<0.05) and Nmda1 N-methyl-D-aspartate receptor (NMDA1 (F= 8.96, p<0.05), which were reverted by acute Ghr 0.3 nmol/ul administration (p ≤0.05). Results show that Ghr 0.3 nmol/µl reverts memory impairment induced by OB in mice and provide information that this effect could be mediate at least in part by CamKII iso2 and NMDA1.