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Fetal Nutrition and Brain Growth

The development of the mammalian brain involves a series of sequential changes that include division, migration, and differentiation of neurons and glia, dendritic arborization, formation of synapses, synthesis and release of neural transmitters and neural hormones, and progressive increase in sensory motor and higher functions. All these changes, which begin before and extend beyond birth, may be affected by prenatal or postnatal nutrition. In this presentation, analysis of two vastly different models of intrauterine growth retardation (IUGR) suggests that there may be a common final pathway through which intrauterine growth failure occurs in both models. This common final pathway may be related to failure of vascular system development, in particular of the placenta during gestation. The first model that produces IUGR by ligation of the uterine artery near term (the so-called Wigglesworth procedure) results in disproportionate fetal growth failure. The brains of these IUGR animals are of normal size, with normal quantities of myelin and gangliosides; however, other organs, such as the liver, are much smaller than expected. The animals are free of behavioral abnormalities, and they are susceptible to hypoglycemia. Maternal malnutrition (protein restriction) is the second most common method of producing IUGR. In this model, the size of the fetus is symmetrically reduced with the fetal brain being reduced in cell number to the same extent as the other organs. Myelination is reduced and the concentration of N-acetyl-neuraminic acid and gangliosides is also reduced. Pups show behavioral abnormalities that persist into adult life. It is hypothesized that malnutrition operates by producing a chronic vascular insufficiency to the uterus and placenta. Maternal malnutrition during pregnancy results in a reduced blood volume expansion that leads to an inadequate increase in cardiac output, followed by a decreased placental blood flow. This decreased placental blood flow will result in a reduced placental size, and at the same time, in a reduced transfer of nutrients, the result being that of fetal growth retardation, although different than that produced by the acute vascular insufficiency of the first model. Postnatally, those animals that have been subject to acute vascular clamping will not survive unless you supply them with exogenous glucose. They have completely depleted glycogen reserves, and they will not survive on their own. If supported, these animals do quite well postnatally without any behavioral deficits. The animals subject to the other type of vascular insult, that is, the abnormal chronic decrease in blood volume and uterine blood flow, survive on their own, but they will show behavioral abnormalities later on. That the above-mentioned models may be generalized to humans has been suggested by the kinds of different outcomes that one sees in populations where fetal malnutrition is rampant, versus populations in which smoking is one of the major causes of reduced fetal growth. Smoking produces an acute vascular