Role of dietary omega-3 PUFA in depression and memory in a rodent model.

EMILIO ZINGERLING; DIEGO MAXIMILIANO WEIGANDT; MARÍA DEL ROSARIO SOLÍS,; MARÍA EMILIA SANTILLÁN; CARLINI, VALERIA PAOLA; BIANCONI SANCIAGO

Congreso; Reunión Anual de la Sociedad de Biociencia; 2020

Background: dietary intake of omega-3 polyunsaturated fatty acids (ω3 PUFA) is reflected in the brain fatty acid composition. These essential nutrients can modify cellular and behavioral processes related to anxiety, depression and memory. In a previous work, we observed that dietary ω3 PUFA deficiency in mouse produced changes associated with the development of depressive-like behavior -like hypermotility and up-regulation of AVP and AVPr1 genes in the hypothalamus and pituitary, respectively- and reduced the hippocampal gene expression of NMDA1, which plays a role in memory formation. On the other hand, ω3 PUFAs excess increased the LTP-related gene CREB1a. Objectives: to assess the effect of dietary ω3 PUFA level on depressive-like behavior and nitric oxide (NO) level in the hippocampus, molecule related to memory formation process. Material and methods: albino Swiss mice were exposed to ω3 PUFA Control (C; soybean oil, 7%), Deficient (D; sunflower oil, 7%) or Excess (E; blend oil; 4.2% cod-liver+2.8% soybean) diet before conception till adulthood, and at this time point, the depressive-like behavior was evaluated through the tail suspension test (TST) in male animals. After that, animals were euthanized and their hippocampi dissected to determine NO level by Griess. Statistics: ANOVA and LSD post hoc test. Results: the immobility time (s) in TST was higher in D group (79.8±14.7) compared to C (43.3±8.7) and E (59.1±10.8) groups (P<0.05 indicated by LSD post hoc). Furthermore, there were no differences in NO level among dietary groups. These results support the hypothesis that ω3 PUFA deficiency induces depressive-like predictive effects, and suggest that the hippocampal NO pathway should not be implicated in the changes on memory gene expression produced by both ω3 PUFA deficiency and excess. Further investigations are needed to better understand the relevance of dietary PUFA ω3 in depression and memory.