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. 1994 Jun;102(Suppl 2):121–124. doi: 10.1289/ehp.94102121

Vulnerable periods and processes during central nervous system development.

P M Rodier 1
PMCID: PMC1567093  PMID: 7925182

Abstract

The developing central nervous system (CNS) is the organ system most frequently observed to exhibit congenital abnormalities. While the developing CNS lacks a blood brain barrier, the characteristics of known teratogens indicate that differential doses to the developing vs mature brain are not the major factor in differential sensitivity. Instead, most agents seem to act on processes that occur only during development. Thus, it appears that the susceptibility of the developing brain compared to the mature one depends to a great extent on the presence of processes sensitive to disruption. Yet cell proliferation, migration, and differentiation characterize many other developing organs, so the difference between CNS and other organs must depend on other properties of the developing CNS. The most important of these is probably the fact that nervous system development takes much longer than development of other organs, making it subject to injury over a longer period.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Arnold A. P., Gorski R. A. Gonadal steroid induction of structural sex differences in the central nervous system. Annu Rev Neurosci. 1984;7:413–442. doi: 10.1146/annurev.ne.07.030184.002213. [DOI] [PubMed] [Google Scholar]
  2. Aschner M., Clarkson T. W. Uptake of methylmercury in the rat brain: effects of amino acids. Brain Res. 1988 Oct 11;462(1):31–39. doi: 10.1016/0006-8993(88)90581-1. [DOI] [PubMed] [Google Scholar]
  3. Burbacher T. M., Rodier P. M., Weiss B. Methylmercury developmental neurotoxicity: a comparison of effects in humans and animals. Neurotoxicol Teratol. 1990 May-Jun;12(3):191–202. doi: 10.1016/0892-0362(90)90091-p. [DOI] [PubMed] [Google Scholar]
  4. Chi J. G., Dooling E. C., Gilles F. H. Gyral development of the human brain. Ann Neurol. 1977 Jan;1(1):86–93. doi: 10.1002/ana.410010109. [DOI] [PubMed] [Google Scholar]
  5. Choi B. H., Lapham L. W., Amin-Zaki L., Saleem T. Abnormal neuronal migration, deranged cerebral cortical organization, and diffuse white matter astrocytosis of human fetal brain: a major effect of methylmercury poisoning in utero. J Neuropathol Exp Neurol. 1978 Nov-Dec;37(6):719–733. doi: 10.1097/00005072-197811000-00001. [DOI] [PubMed] [Google Scholar]
  6. Christensen S., Ottosen P. D., Olsen S. Severe functional and structural changes caused by lithium in the developing rat kidney. Acta Pathol Microbiol Immunol Scand A. 1982 Jul;90(4):257–267. doi: 10.1111/j.1699-0463.1982.tb00090_90a.x. [DOI] [PubMed] [Google Scholar]
  7. Daston G. P., Kavlock R. J., Rogers E. H., Carver B. Toxicity of mercuric chloride to the developing rat kidney. I. Postnatal ontogeny of renal sensitivity. Toxicol Appl Pharmacol. 1983 Oct;71(1):24–41. doi: 10.1016/0041-008x(83)90042-x. [DOI] [PubMed] [Google Scholar]
  8. EAYRS J. T. The cerebral cortex of normal and hypothyroid rats. Acta Anat (Basel) 1955;25(2-4):160–183. doi: 10.1159/000141068. [DOI] [PubMed] [Google Scholar]
  9. Fox M. W. Neuro-behavioral ontogeny. A synthesis of ethological and neurophysiological concepts. Brain Res. 1966 Jul;2(1):3–20. doi: 10.1016/0006-8993(66)90059-x. [DOI] [PubMed] [Google Scholar]
  10. Gavin C. E., Kates B., Hoffman G. E., Rodier P. M. Changes in the reproductive system following acute prenatal exposure to ethanol or methylazoxymethanol in the rat: I. Effects on immunoreactive LHRH cell number. Teratology. 1994 Jan;49(1):13–19. doi: 10.1002/tera.1420490104. [DOI] [PubMed] [Google Scholar]
  11. Hohmann A., Creutzfeldt O. D. Squint and the development of binocularity in humans. Nature. 1975 Apr 17;254(5501):613–614. doi: 10.1038/254613a0. [DOI] [PubMed] [Google Scholar]
  12. Johanson C. E. Permeability and vascularity of the developing brain: cerebellum vs cerebral cortex. Brain Res. 1980 May 19;190(1):3–16. doi: 10.1016/0006-8993(80)91155-5. [DOI] [PubMed] [Google Scholar]
  13. Miller J. C., Friedhoff A. J. Prenatal neurotransmitter programming of postnatal receptor function. Prog Brain Res. 1988;73:509–522. doi: 10.1016/S0079-6123(08)60523-3. [DOI] [PubMed] [Google Scholar]
  14. Rakic P. Neuron-glia relationship during granule cell migration in developing cerebellar cortex. A Golgi and electronmicroscopic study in Macacus Rhesus. J Comp Neurol. 1971 Mar;141(3):283–312. doi: 10.1002/cne.901410303. [DOI] [PubMed] [Google Scholar]
  15. Rakic P., Sidman R. L. Histogenesis of cortical layers in human cerebellum, particularly the lamina dissecans. J Comp Neurol. 1970 Aug;139(4):473–500. doi: 10.1002/cne.901390407. [DOI] [PubMed] [Google Scholar]
  16. Rodier P. M. Chronology of neuron development: animal studies and their clinical implications. Dev Med Child Neurol. 1980 Aug;22(4):525–545. doi: 10.1111/j.1469-8749.1980.tb04363.x. [DOI] [PubMed] [Google Scholar]
  17. Schull W. J., Norton S., Jensh R. P. Ionizing radiation and the developing brain. Neurotoxicol Teratol. 1990 May-Jun;12(3):249–260. doi: 10.1016/0892-0362(90)90096-u. [DOI] [PubMed] [Google Scholar]
  18. Wiggins R. C. Myelin development and nutritional insufficiency. Brain Res. 1982 Jun;257(2):151–175. doi: 10.1016/0165-0173(82)90016-9. [DOI] [PubMed] [Google Scholar]

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