Reduced maternal behavior caused by gestational stress is predictive of life span changes in risk-taking behavior and gene expression due to altering of the stress/anti-stress balance

Gestational folic acid supplementation does not affects the maternal behavior and the early development of rats submitted to neonatal hypoxia‐ischemia but the high supplementation impairs the dam's memory and the Na+, K+ ‐ ATPase activity in the pup's hippocampus

“…Also, somatosensory inputs from the pups during the days contribute to the augmenting expression of maternal behavior (Pedersen et al, 1995). Contrary to our findings, Gatta et al, (2018) observed a decreased in the activity maternal behavior (measured by feeding, licking, grooming and carrying the pups) during the first 5 days in dams that were submitted to a perinatal stress protocol. It is also known that treatment with antipsychotic during pregnancy disrupt the active components of maternal behavior by decreasing the time feeding the pups and increasing the latency to get the pups and start to build the nest (Li, 2015).…”

Perinatal Stress Programs Sex Differences in the Behavioral and Molecular Chronobiological Profile of Rats Maintained Under a 12-h Light-Dark Cycle

“…The active behavior of the mother (nursing behavior, grooming, licking, and carrying pups) was scored and the data obtained were expressed as percentages with respect to the total number of observations. Since gestational stress induces a reduction of maternal behavior (Gatta et al, 2018), we refer to the whole procedure as PRS having a prenatal and postnatal effect). In the present study, only male and female offspring from dams presenting a stress-reduced maternal behavior (with a cutoff below 40% of maternal care in the PRS group vs. a cutoff above 60% of maternal care in the control group), and from litters of 10–14 rats with a similar number of males and females, were used.…”

“…Exposure to stressful events in early life strongly programs an individual’s phenotype and adaptive capabilities by modifying reactive (Weaver et al, 2004; Seckl, 2008; Brunton et al, 2011; Maccari et al, 2017) as well as predictive adaptation (Van Reeth et al, 2000; Maccari and Morley-Fletcher, 2007). A well-characterized animal model of early programming of stress response is the PRS model in the rat (Maccari et al, 1995; for a review see Maccari et al, 2017), in which exposure to gestational stress and altered maternal behavior programs a life-long disruption in the reactive adaptation such as a hyperactive response to stress and a defective feedback of the hypothalamus-pituitary-adrenal (HPA) axis (Vallée et al, 1999; Gatta et al, 2018) together with long-lasting modifications in stress/anti-stress gene expression balance in the hippocampus (Mairesse et al, 2015; Gatta et al, 2018). The changes induced by PRS in predictive adaptation include a profound alteration of the sleep-wake cycle architecture together with increased sleep fragmentation when the animals reach adulthood (Dugovic et al, 1999; Mairesse et al, 2013) and alterations in the rhythm of plasma corticosterone secretion (Koehl et al, 1999).…”

The Stimulation of Neurogenesis Improves the Cognitive Status of Aging Rats Subjected to Gestational and Perinatal Deficiency of B9–12 Vitamins

“…Globally, the level of expression of the N-methyl D-aspartate receptor 1 (NMDAR1) and the post-synaptic density-95 (PSD-95) were negatively correlated to the deficient diet alone, and positively correlated to hypoxia. This indicates that the deficiency in B-vitamins affected the hippocampus status in terms of circuit plasticity and that this aspect was maintained during the lifespan, as the Barker theory described for developmental or neonatal events leading to long term positive or negative effects [45,46]. At the same time, the hypoxia-stimulated-mechanism occurring in the same neonatal period could give advantages to receptive circuits such as the hippocampus leading to maintain a long term efficient plasticity even under transient deficiency in B-vitamins.…”