Dietary n-3 fatty acid deficiency induces depression-related behavior mediated by vasopressin

SANTIAGO BIANCONI; MARIA BELEN PORETTI; GIULIA MAESTRI; MARIA EMILIA SANTILLÁN; ROSARIO SOLIS; HELGI B. SCHIOTH; MICHAEL WILLIAMS; GRACIELA STUTZ; VALERIA PAOLA CARLINI

Mar del Plata

Congreso; LVIII Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2016

SAIC, SAI, SAFE

Dietary n-3 fatty acid deficiency induces depression-related behavior mediated by vasopressinAdverse fetal and postnatal conditions, such as nutritional imbalance, can predispose to psychiatric disorder developmentinthe adulthood. Omega-3 (n-3) polyunsaturated fatty acid (PUFA)offer can modify the central nervous system development andfunction. Thus, we propose to study the effect of long term exposition to different dietary levels of n-3 PUFA, from gestation to adulthood, among depression-related parameters. Three groups of albino Swiss female mice (during gestation-lactation) and then their male offspring (during weaning-adulthood; n~10per group) were fed with C (control, adequate in n-3 diet; 7% soya oil;n-3:0.57%; n-6/n-3: 5.7), D (deficient in n-3 diet; 7% sunfloweroil; n-3: 0%;n-6/n-3: 0) or E (excessive in n-3 diet; 7% blend oil: cod liver 60% + soya 40%; n-3: 1.25%; EPA 0.43% y DHA 0.32%n-6/n-3: 1.29). At postnatal day 63,open field test was performed in order to study locomotor activity. Then, animals were sacrificed to determine plasma corticosterone levels by ELISA and gene expression of vasopressin (AVP) and corticotropin releasing hormone (CRH) -in hypothalamus- and their receptors AVPr1b, CRHR1 and CRHR2 -in the pituitary gland- by RT-qPCR. The D group showed higher locomotor activity (crossing number: D 415 ± 37 vs C 195 ± 25; p<0.05) and gene expression of AVP(F(23,2)=4.96; p<0.05 vs C y E) and its receptor (F(31,2)=7.27; p<0.05 vs C y E). Furthermore, the messenger level of CRH and its receptors as well as plasma corticosterone concentration did not change significantly. Our results show that n-3 PUFA deficiency could selectively modify the hypothalamic-pituitary-adrenal axis function and induce depression-related behavior.