Newborn of altricial species maintain functional gustatory communication with the mother because the neural substrate and the capacity to discriminate and promote gustofacial responses are already operating. Because little is known about the effects of perinatal food restriction upon gustatory neuronal brain stem structures, we characterized neuronal Golgi-Cox alterations of the solitary tract rostral portion (NSTr) where gustatory information is known to convey in neonatal Wistar rats. Pre-and neonatally undernourished rats exhibited a general reduction in the number and extension of distal dendrites particularly in small neurons but little effect upon perikarya measurements of the NSTr neuronal population. By contrast, in nutritional and sensory rehabilitated rats the number of distal dendrites increased, although the dendritic extensions were less affected compared to perinatally underfed and control subjects. The data indicate that perinatal food restriction interferes with the NSTr dendritic arbor organization, while nutritional and sensorial rehabilitation given by normally lactating dams induced plastic changes presumably modifying the integrative processes underlying early taste discriminative capabilities. Moreover, since perinatal food restriction is a powerful stressor influence and the NST forms a part of a complex system underlying adaptive stress responses, the neuronal alterations observed here may be partly due to this noxious perinatal influence.

In the rat, perinatal food and maternal deprivation provoke long-lasting effects upon the retrieving responses of dams to displaced pups. In the current study, the retrieving latency and the disruption in the body area of pups chosen by the mother to transport them to a new location was investigated on days 4, 8 and 12 postpartum in lactating Wistar rats. Rats, neonatally underfed by daily (12 h) mother-litter separation in an incubator from days 1 to 23 postpartum, exhibited prolonged retrieving latencies and disruption in the body area of young ones chosen by the dam to transport them to the nest. Furthermore, neonatally underfed dams frequently transported pups in a rude manner eliciting sonic distress cries from them compared to control mothers. These findings are possibly relevant to understand the impact of epigenetic influences on offspring brain and physiological maturation partly mediated through maternal care.

Cell alterations in the central nervous system are consistent consequences of early undernourishment. Because little is known about the effects of neonatal udernourishment upon the main olfactory bulb (OB) in Golgi-Cox stained material, we evaluated the total OB cross-sectional area, the area of individual OB layers, and the area of type II mitral cells perikarya and their dendritic processes in undernourished Wistar rats of 7, 14, and 21 days of age. Data showed that neonatal undernourishment reduced both the OB and the individual layers areas; minimal perikarya effects and significant reductions in the number and extension of MC dendrites. Although macroneurons are formed prenatally, neonatal undernourishment at critical periods may have long-lasting effects that interfere with the functional maturity of the OB. These findings may have relevant consequences for early odor discrimination of the offspring, since olfaction is a fundamental sensorial avenue for newborn adaptive responses and maternal care.

Golgi-Cox-stained bipolar cells of the medial superior olive (MSO) were analyzed in control and undernourished Wistar strain rats at 12, 20, 30 and 40 days of age. Undernutrition significantly reduced the number of dendrites and the extension of ipsilateral dendritic prolongations, with no effects upon the cross-sectional somal area and minimal alterations in the corresponding contralateral dendritic branches. The data suggest that in underfed rate, afferents from the receptors projecting to the MSO via the anteroventral cochlear nuclei may cause an imbalance in the binaural interactions which occur between the axon terminals and the ipsilateral and contralateral dendritic arbors of MSO neurons.

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