Nutritional influences on adrenal chromaffin cell development: Comparison with central neurons

Abstract

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-bio-synthetic enzymes tyrosine hydroxylase and phenyletha-nolamine 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 adrenal 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 (<10%) 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. © 1988 International Pediatrics Research Foundation, Inc.