Accéder au contenu
Merck

Neurodevelopment and Cognitive Impairment in Parents and Progeny of Perinatal Dietary Protein Deficiency Models.

Frontiers in neuroscience (2019-09-26)
Nosarieme O Abey, Osaretin A T Ebuehi, Ngozi O A Imaga
RÉSUMÉ

There is an absolute dependence of the concept of development on supply of adequately balanced nutrients especially during the perinatal age which is critical to development. Therefore, an upgraded nutrition is specially required during gestation and lactation, as this is the critical period of neurodevelopment. This study sought to investigate the effect of protein deficiency during gestation (F0) and lactation through to adolescence on neurological functions of subsequent (F1 and F2) generations, establishing the possible consequential mechanistic association. Rats in four groups were fed different rations of protein diets (PD) as formulated: 21% PD, 10% PD, 5% PD and control diet (standard rat chow, containing 16-18% protein), from adolescent through to gestation and lactation, next generations were weaned to the maternal diet group. Neurobehavioral studies (which include; Surface righting reflex, Negative geotaxis, Learning and Memory tests), brain oxidative stress and quantification of serotonin and dopamine levels in the brain were conducted. Result shows significantly altered neurobehavior, reflected in the reduction of reflex response and postural reaction score at P ≤ 0.05. There was also a transgenerational cognitive impairment of brain function in the F-generations, following perinatal protein malnutrition as shown in the Y-maze result, measuring spatial memory and Morris water maze result (cognition), providing a background for the observed sensorimotor response. The significant increase in dopamine level, decrease in the antioxidant capacity of the protein deficient brain groups are consistent with significantly altered serotonin system, critical to neurodevelopment and functional activities of learning and memory. Therefore, persistent early life protein deficiency mediates dysfunction in neurodevelopment and this involves life-long changes in key neurotransmitters and the brain redox status underlying the neurobehavioral display.