Literature DB >> 2905035

Nutritional influences on adrenal chromaffin cell development: comparison with central neurons.

C Lau1, F J Seidler, A M Cameron, H A Navarro, J M Bell, J Bartolome, T A Slotkin.   

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-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 weights 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 (less than 10%) in brain tyrosine hydroxylase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1988        PMID: 2905035     DOI: 10.1203/00006450-198811000-00009

Source DB:  PubMed          Journal:  Pediatr Res        ISSN: 0031-3998            Impact factor:   3.756


  13 in total

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Authors:  Theodore A Slotkin; Frederic J Seidler
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3.  Overexpression of the high affinity choline transporter in cortical regions affected by Alzheimer's disease. Evidence from rapid autopsy studies.

Authors:  T A Slotkin; C B Nemeroff; G Bissette; F J Seidler
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4.  Developmental neurotoxic effects of chlorpyrifos on acetylcholine and serotonin pathways in an avian model.

Authors:  Theodore A Slotkin; Frederic J Seidler; Ian T Ryde; Joseph Yanai
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5.  Is fipronil safer than chlorpyrifos? Comparative developmental neurotoxicity modeled in PC12 cells.

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6.  Silver nanoparticles compromise neurodevelopment in PC12 cells: critical contributions of silver ion, particle size, coating, and composition.

Authors:  Christina M Powers; Appala R Badireddy; Ian T Ryde; Frederic J Seidler; Theodore A Slotkin
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7.  Developmental neurotoxicity of chlorpyrifos: what is the vulnerable period?

Authors:  Dan Qiao; Frederic J Seidler; Stephanie Padilla; Theodore A Slotkin
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8.  Fetal chlorpyrifos exposure: adverse effects on brain cell development and cholinergic biomarkers emerge postnatally and continue into adolescence and adulthood.

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Journal:  Environ Health Perspect       Date:  2003-04       Impact factor: 9.031

9.  Chlorpyrifos affects phenotypic outcomes in a model of mammalian neurodevelopment: critical stages targeting differentiation in PC12 cells.

Authors:  Ruth R Jameson; Frederic J Seidler; Dan Qiao; Theodore A Slotkin
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10.  Silver impairs neurodevelopment: studies in PC12 cells.

Authors:  Christina M Powers; Nicola Wrench; Ian T Ryde; Amanda M Smith; Frederic J Seidler; Theodore A Slotkin
Journal:  Environ Health Perspect       Date:  2010-01       Impact factor: 9.031

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