Nutritional Influences on Adrenal Chromaffin Cell Development: Comparison with Central Neurons

Abstract

ABSTRAm. Neurotransmitter systems in the developing brain are generally protected from growth retardation associated with nutritional deprivation. To investigate if such protective mechanisms extend to similar tissues in the peripheral sympathetic system, maturation of the chromaffin cells of the adrenal medulla and development of their centrally derived splanchnic innervation were evaluated in rats whose nutritional status had been altered during the neonatal period by increasing (16-17 pups/ litter) or decreasing (five to six pups/litter) the litter size from the standard (11-12 pups/litter). Ontogeny of adrenal catecholamine stores and activities of catecholamine-biosynthetic enzymes tyrosine hydroxylase and phenylethanolamine N-methyltransferase were monitored, along with activity of choline acetyltransferase, a marker enzyme for the preganglionic neurons innervating the chromaffin cells. Neonatal nutritional deprivation slowed body weight gain and retarded development of the chromaffin cells, as evidenced by subnormal catecholamine stores, tyrosine hydroxylase and phenylethanolamine N-methyltransferase activities. The effects persisted despite the complete recovery of body wr ights postweaning. The developmental alterations were not caused by overcrowding stress, as plasma corticosterone levels were not elevated in the large litter group. Neonatal nutritional enrichment promoted body weight gain but failed to enhance development of adrer.al catecholamines; tyrosine hydroxylase and phenylethanolamine N-methyltransferase activities were elevated only in the preweaning period. In contrast to effects on the chromaffin cells, altered neonatal nutritional status had only minor, transient effects on the development of the centrally derived cholinergic innervation of the adrenal and produced only small changes (~1 0 % ) in brain tyrosine hydroxylase activity. These results suggest that, unlike central transmitter systems, maturation of chromaffin cells is adversely affected by neonatal nutritional deprivation; ontogenetic gains may already be close to optimum at normal nutritional status. (Pediatr Res 24: 583-587, 1988) Abbreviation ANOVA, analysis of variance Growth and development of the newborn are influenced profoundly by nutritional status (1-3). Thus, in rats, manipulation of litter size produces marked differences in growth rates that are associated with changes in cell replication and differentiation, in structure and size of individual tissues, and in maturation of organ function. In contrast, development of the CNS is spared during neonatal nutritional deprivation and shows little or no enhancement of maturation during overnourishment (4). Recent studies confirm that selective intracellular and multicellular mechanisms participate in this process: maturational patterns of the ornithine decarboxylase/polyamine system, which regulates macromolecule synthesis during development, are maintained in brain regions at the expense of disruption of the same pathway in other organs (4). In fact, neural signals de...

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“…TH activity was measured using [ 14 C]tyrosine as a substrate and trapping the evolved 14 CO 2 after coupled decarboxylation with dopa decarboxylase (Lau et al, 1988). Homogenates were sedimented at 26 000g for 10 min to remove storage vesicles containing catecholamines, which interfere with TH activity, and assays were conducted with 100 ml aliquots of the supernatant solution in a total volume of 550 ml.…”

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