Early life adversities or high fat diet intake reduce cognitive function and alter BDNF signaling in adult rats: Interplay of these factors changes these effects

Abstract

Environmental factors, like early exposure to stressors or high caloric diets, can alter the early programming of central nervous system, leading to long-term effects on cognitive function, increased vulnerability to cognitive decline and development of psychopathologies later in life. The interaction between these factors and their combined effects on brain structure and function are still not completely understood. In this study, we evaluated long-term effects of social isolation in the prepubertal period, with or without chronic high fat diet access, on memory and on neurochemical markers in the prefrontal cortex of rats. We observed that early social isolation led to impairment in short-term and working memory in adulthood, and to reductions of Na(+),K(+)-ATPase activity and the immunocontent of phospho-AKT, in prefrontal cortex. Chronic exposure to a high fat diet impaired short-term memory (object recognition), and decreased BDNF levels in that same brain area. Remarkably, the association of social isolation with chronic high fat diet rescued the memory impairment on the object recognition test, as well as the changes in BDNF levels, Na(+),K(+)-ATPase activity, MAPK, AKT and phospho-AKT to levels similar to the control-chow group. In summary, these findings showed that a brief social isolation period and access to a high fat diet during a sensitive developmental period might cause memory deficits in adulthood. On the other hand, the interplay between isolation and high fat diet access caused a different brain programming, preventing some of the effects observed when these factors are separately applied.

Adverse maternal environment and western diet impairs cognitive function and alters hippocampal glucocorticoid receptor promoter methylation in male mice

“…later in life. Pervious animal models by others have not recapitulated these human findings entirely (Tozuka et al, 2010; Zieba, Uddin, Youngson, Karl, & Morris, 2019) or found that the combination of two environmental insults rescued memory impairment (Arcego et al, 2016). Importantly, these other animal models employed different types and timing of environmental stressors on the offspring.…”

“…An adverse maternal environment (AME) and the consumption of a western diet (WD) starting in early childhood affect health later in life (Alastalo et al, 2013; Francis & Stevenson, 2013). More specifically, human and animal studies reveal a strong association between exposure to either an AME or WD and the development of cognitive impairment and depressive disorders later in life (Alastalo et al, 2013; Arcego et al, 2016; Francis et al, 2013). AME has been shown to decreased learning and memory while maternal WD consumption has been shown to alter memory and depression in offspring (Alastalo et al, 2013; Arcego et al, 2016; de Kloet, Joels, & Holsboer, 2005; Francis et al, 2013).…”

“…More specifically, human and animal studies reveal a strong association between exposure to either an AME or WD and the development of cognitive impairment and depressive disorders later in life (Alastalo et al, 2013; Arcego et al, 2016; Francis et al, 2013). AME has been shown to decreased learning and memory while maternal WD consumption has been shown to alter memory and depression in offspring (Alastalo et al, 2013; Arcego et al, 2016; de Kloet, Joels, & Holsboer, 2005; Francis et al, 2013). However, while AME and WD are often studied separately, these two conditions are often experienced together and over the course of a lifetime.…”

Differences in the persistence of spatial memory deficits induced by a chronic stressor in adolescents compared to juveniles

“…Some of these studies have, however, assessed object recognition memory and spatial memory. For example, in one study pre‐pubertal stress was found to impair object recognition in adult males rats (Arcego et al, ). In the present study, prepubertal stress did not affect object recognition memory either 6‐days or 6‐weeks after the stress exposure had terminated (with the latter time point being in early adulthood).…”

Down-Regulation of Hippocampal Genes Regulating Dopaminergic, GABAergic, and Glutamatergic Function Following Combined Neonatal Phencyclidine and Post-Weaning Social Isolation of Rats as a Neurodevelopmental Model for Schizophrenia

“…In particular, neonatal PCP induces long-term locomotor abnormality, cognitive dysfunction (Depoortere et al, 2005), impaired sensorimotor gating (Wang et al, 2001) and loss of parvalbumin-containing GABAergic neurones accompanied by changes in autophagy (Radonjic et al, 2013; Jevtic et al, 2016), reminiscent of features of schizophrenia. As no single rodent paradigm completely reproduces the diverse schizophrenia symptom profile, groups have started to characterize “dual-hit” models in rodents to produce more comprehensive and robust deficits, in particular of cognitive and negative features (Ashby et al, 2010; Gilabert-Juan et al, 2012; Lim et al, 2012; Giovanoli et al, 2013; Gaskin et al, 2014; Arcego et al, 2016). …”