RESUMEN
We investigated the effect of a chronic palatable diet rich in simple sugars on memory of different degrees of emotionality in male adult rats, and on hippocampal plasticity markers in different stages of development. On postnatal day (PND) 21, 45 male Wistar rats were divided in two groups, according to their diet: (1-Control) receiving standard lab chow or (2-Palatable Diet) receiving both standard chow plus palatable diet ad libitum. At PND 60, behavioral tests were performed to investigate memory in distinct tasks. Hippocampal plasticity markers were investigated at PND 28 in half of the animals, and after the behavioral tests. Palatable diet consumption induced an impairment in memory, aversive or not, and increased Na+ , K+ -ATPase activity, both at PND 28, and in the adulthood. Synaptophysin, brain-derived neurotrophic factor (BDNF), and protein kinase B (AKT), and phosphorylated AKT were reduced in the hippocampus at PND 28. However, at PND 75, this diet consumption led to increased hippocampal levels of synaptophysin, spinophilin/neurabin-II, and decreased BDNF and neuronal nitric oxide synthase. These results showed a strongly association of simple sugars-rich diet consumption during the development with memory impairments. Plasticity markers are changed, with results that depend on the stage of development evaluated.
RESUMEN
During development, the brain goes through fundamental processes, including organization of neural networks and plasticity. Environmental interventions may change initial brain programming, leading to long-lasting effects and altering the susceptibility to psychopathologies, including depression disorder. It is known that depression is a psychiatric disorder with a high prevalence worldwide, including high rates among adolescents. In this study, we evaluated whether social isolation in the prepubertal period and chronic use of high-fat diet (HFD) may induce depressive-like behavior in male adult rats. We also investigated hippocampal plasticity markers and neurotransmitter systems. We found both social isolation and HFD induced a depressive-like behavior in the forced swimming task. Moreover, chronic HFD reduced synaptic markers in hippocampus, demonstrated by reductions in ßIII-tubulin (neuronal marker), PSD-95, SNAP-25, and neurotrophin-3. The HFD group also presented decreased glutamatergic and GABAergic receptors subunits. On the other hand, stress affected hippocampal brain-derived neurotrophic factor (BDNF) signaling pathways, and increased expression of subunit of the NMDA receptor (NR2A). Both factors (stress and diet) decreased GR in the hippocampus without affecting plasma corticosterone at basal levels. Interactions between early stress and HFD access were observed only in the BNDF receptor (tropomyosin receptor kinase B; TrkB) and synaptophysin. In summary, these findings showed that a brief social isolation and chronic HFD, during a sensitive developmental period, cause depressive-like behavior in adulthood. The mechanisms underlying these behavioral effects may involve changes in the levels of synaptic proteins in hippocampus: HFD consumption appears to affect synaptic markers, while social isolation affected BDNF signaling more significantly.