RESUMEN
Stress during development can shift the typical developmental trajectory. Maternal stress prior to conception has recently been shown to exert similar influences on the offspring. The present study questioned if a consistent maternal stressor prior to conception (elevated platform stress) would impact the pre-weaning development of offspring brain and behavior, and if maternal care was vulnerable to this experience. Adult female Long-Evans rats were subjected to elevated platform stress for 27â¯days prior to mating with non-stressed males. Maternal care was monitored, and pups were assessed in two tests of early behavioral development, negative geotaxis and open field. Pups were perfused at weaning and their brains were extracted and stained with Cresyl Violet, allowing gross measurements of cortical and subcortical structures and estimates of neuron density. Main findings indicate that a change in prefrontal cortical thickness is evident despite no change in maternal care. Female offspring show a decrease in medial-dorsal thalamus size. The current study failed to find an effect of maternal preconception stress on early behavioral development. These results suggest that the PFC, and likely behavior dependent on the PFC, is vulnerable to maternal preconception stress and that a strong sex effect is evident. Further studies should examine how such offspring fare using a lifespan model and investigate potential mechanisms responsible for these effects.
Asunto(s)
Conducta Materna , Corteza Prefrontal/crecimiento & desarrollo , Corteza Prefrontal/patología , Estrés Psicológico/patología , Animales , Conducta Animal , Recuento de Células , Epigénesis Genética , Femenino , Masculino , Embarazo , Ratas Long-Evans , Tálamo/crecimiento & desarrollo , Tálamo/patologíaRESUMEN
Iron deficiency has a critical impact on maturational mechanisms of the brain and the damage related to neuroanatomical parameters is not satisfactorily reversed after iron replacement. However, emerging evidence suggest that enriched early experience may offer great therapeutic efficacy in cases of nutritional disorders postnatally, since the brain is remarkably responsive to its interaction with the environment. Given the fact that tactile stimulation (TS) treatment has been previously shown to be an effective therapeutic approach and with potential application to humans, here we ask whether exposure to TS treatment, from postnatal day (P) 1 to P32 for 3min/day, could also be employed to prevent neuroanatomical changes in the optic nerve of rats maintained on an iron-deficient diet during brain development. We found that iron deficiency changed astrocyte, oligodendrocyte, damaged fiber, and myelinated fiber density, however, TS reversed the iron-deficiency-induced alteration in oligodendrocyte, damaged fiber and myelinated fiber density, but failed to reverse astrocyte density. Our results suggest that early iron deficiency may act by disrupting the timing of key steps in visual system development thereby modifying the normal progression of optic nerve maturation. However, optic nerve development is sensitive to enriching experiences, and in the current study we show that this sensitivity can be used to prevent damage from postnatal iron deficiency during the critical period.