Clonidine treatment during gestation prevents functional deficits induced by prenatal malnutrition in the rat visual cortex.

It has been shown that prenatal malnutrition results at birth in increased concentration of noradrenaline (NA) in the brain. Besides, it is known that NA is an important regulator of normal regressive processes occurring during synaptogenesis such as cell death, axonal pruning and synaptic elimination. The present study was designed to investigate (i) whether prenatal malnutrition enhances the NA release in the visual cortex and (ii) whether or not chronic administration of clonidine during gestation may prevent long-term deleterious effects of fetal malnutrition on functional properties of interhemispheric connections of the visual cortex and on the interhemispheric asymmetry of visual evoked responses. Prenatal malnutrition was induced by restricting food consumption to pregnant rats from Day 8 postconception to parturition. Results show that at birth, prenatally malnourished rats had higher NA release than normals. At 45-50 days of age, the malnourished group exhibited (a) reduced peak-to-peak amplitude and diminished extent of the projecting field of transcallosal evoked responses, and (b) abolished interhemispheric asymmetry of visual evoked responses. Clonidine administration to malnourished mothers from Day 14 postconception to parturition (10 g/kg/day s.c.), prevented in the offspring disorders induced by prenatal malnutrition on cortical NA release, on interhemispheric connectivity of visual areas and on interhemispheric bioelectrical asymmetry, probably by restoring the normal trophic role of NA during synaptogenesis. Results are discussed in relationship to normal regressive events occurring during early brain development.