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Abstract
A great body of evidence indicates that malnutrition early in life induces central noradrenergic hyperactivity (CNH). On the other hand, it is known that noradrenaline (NA) is an important regulator of the regressive processes occurring during synaptogenesis such as cell death, axonal pruning and synaptic elimination. This leads to the hypothesis that some of the morphofunctional modifications induced by malnutrition on the brain could be due, at least in part, to an increase of NA activity during the period of accelerated brain growth. This study evaluates whether early reduction of CNH by the alpha-2 presynaptic adrenoreceptor agonist clonidine, prevents long-term morphofunctional deficits induced by protein-energy malnutrition in the rat. Results of experiments performed on 45 day-old malnourished animals that received clonidine during the suckling period, show that the pharmacological treatment prevented: (i) deficits in both NA levels and NA release in the visual cortex; (ii) deficit in brain weight but not in body weight; and (iii) reduction of the normal brain interhemispheric asymmetry of visual cortical evoked potentials. It is suggested that administration of clonidine early in life prevents brain morphofunctional deficits by malnutrition, by restoring the normal tropic role of NA during synaptogenesis.