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  1. Home
  2. Browse by Author

Browsing by Author "Hernandez, A"

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    Effects of mild protein prenatal malnutrition and subsequent postnatal nutritional rehabilitation on noradrenaline release and neuronal density in the rat occipital cortex
    (1999) Soto-Moyano, R; Fernandez, V; Sanhueza, M; Belmar, J; Kusch, C; Perez, H; Ruiz, S; Hernandez, A
    There is evidence that severe malnutrition started during gestation and continued through lactation affects adversely the morphologic development of the neocortex leading to increased neuronal cell packing density and decreased dendritic branching. Nevertheless, the effect of purely mild protein prenatal malnutrition on neocortical development remains rather unexplored. This study evaluates the effects of mild protein prenatal malnutrition (8% casein diet, calorically compensated by carbohydrates) and subsequent postnatal nutritional rehabilitation (25% casein diet) on: (i) the potassium-induced release of [H-3]-noradrenaline (NA) in occipital cortex slices obtained from 1- and 22-day-old pups; and (ii) the packing density of neurons in lateral, dorso-lateral and dorsal regions of the occipital cortex of 22-day-old pups by using the optical dissector method. The experiments were performed in rats normally fed during gestation and lactation (G(+)L(+)), malnourished during gestation but rehabilitated during lactation (G(-)L(+)) and malnourished during gestation and lactation (G(-)L(-)). At day 1 of age, no significant differences in body and brain weights were observed between prenatally well-nourished and malnourished pups. Nevertheless, at this early age, pups born from mothers submitted to the 8% casein diet had significantly higher cortical net percent NA release than pups born from mothers receiving the 25% casein diet. At weaning (22 days of age) G(-)L(+) rats had, compared to the G(+)L(+) group, similar body weight, brain weight and [H-3]-NA release values, but significantly higher neuron density scores in the lateral region of the occipital cortex. In contrast, at 22 days of age, G(-)L(-) rats exhibited, compared to G(+)L(+) animals, significant deficits in body and brain weights as well as significant increases in cortical net percent NA release together with enhanced packing density of neurons in the lateral, dorso-lateral and dorsal regions of the occipital cortex. Moreover, in G(-)L(-) animals was not found the laterodorsal histogenetic gradient of neuronal cell packing density observed in G(+)L(+) rats. Results suggest that mild prenatal malnutrition per se is able to induce deleterious effects on cortical neuronal density, in spite of nutritional rehabilitation during lactation, through a mechanism involving central NA hyperactivity during gestation. Prosecution of malnutrition after birth magnifies both neurochemical and morphometric disorders. (C) 1999 Published by Elsevier Science B.V. All rights reserved.
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    Malnutrition early in life impairs alpha-2 adrenoreceptor regulation of noradrenaline release in the rat cerebral cortex
    (1996) Belmar, J; Carreno, P; Hernandez, A; SotoMoyano, R
    Experimental studies have shown that malnutrition early in life results in enhanced release of noradrenaline (NA) in the brain. The disturbed mechanism underlying this neurochemical disorder is pearly understood. To test the possibility that early malnutrition could disrupt the feedback mechanism regulating the release of NA at central axon terminals, the ability of the adrenoreceptor agonist clonidine to depress NA overflow was studied in rat cortex slices arising from malnourished rats. Protein-energy malnutrition was induced by increasing litter size from 8 to 18 pups per nurse. Results show that clonidine (5 x 10(-6) M) induced a significant decrease of the spontaneous release of NA in occipital cortex slices obtained from 23-24 day-old normal rats and of the potassium-evoked release of NA in slices arised from normal animals of 45-50 days of age. On the contrary, clonidine induced a significant increase of both the spontaneous and evoked outflow of the neurotransmitter in slices arised from malnourished rats of the two ages. Results indicate that protein-energy malnutrition impairs the alpha-2 receptor mechanisms regulating central NA overflow, probably by altering during development the quantity and/or quality of the adrenoreceptor population.

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