Nature 314, 751 - 752 (25 April 1985); doi:10.1038/314751a0

Central nervous system and peripheral nerve growth factor provide trophic support critical to mature sensory neuronal survival

Eugene M. Johnson Jr & Henry K. Yip

Department of Pharmacology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA

Primary sensory neurones in cranial and dorsal root ganglia (DRG) of adult animals are generally thought to be maintained through connections with their peripheral (but not central) targets by trophic factor(s) other than nerve growth factor (NGF)¹. Damage to the peripheral process of sensory neurones results in a dramatic response or even death of the neurones, whereas axotomy (cutting) of the central process does not initiate profound reaction in these neurones. The development and maintenance of neurones are highly dependent on a supply of trophic agents produced by targets and retrogradely transported via the peripheral process to the cell body². NGF deprivation in fetal rodents produced either by exogenously administered antibodies or by those of maternal origin, results in death of DRG²⁻⁵ and of some cranial sensory neurones⁶. However, as chronic NGF deprivation in neonatal or adult rodents produces little or no cell death⁷⁻¹⁰, it has been assumed that some other trophic factor(s) derived from the peripheral target sustains sensory neurones in postnatal life. By inducing NGF deprivation by autoimmunizing guinea pigs with mouse NGF and/or by cutting the central root (process) of a DRG, we demonstrate here that under certain conditions DRG neurones require NGF and centrally derived trophic support. Our results indicate that sensory neurones are maintained by the trophic support provided by both peripheral and central targets. This support is mediated by NGF and other as yet unidentified trophic factors. The relative importance of the two target fields and NGF compared with other trophic factors changes during development.

References

1.	Lieberman, A. R. Int. Rev. Neurobiol. 14, 49−124 (1971). | PubMed | ChemPort |
2.	Hamburger, V. & Oppenheim, R. W. Neurosci. Comment. 1, 39−55 (1982).
3.	Gorin, P. D. & Johnson, E. M. Proc. natn. Acad. Sci. U.S.A. 76, 5382−5386 (1979). | ChemPort |
4.	Johnson, E. M., Gorin, P. D., Brandeis, L. D. & Pearson, J. Science 210, 916−918 (1980). | PubMed | ISI | ChemPort |
5.	Aloe, L., Cozzani, C., Calissano, P. & Levi-Montalcini, R. Nature 291, 413−415 (1981). | PubMed | ISI | ChemPort |
6.	Pearson, J., Johnson, E. M. & Brandeis, L. Devl Biol. 96, 32−36 (1983). | ChemPort |
7.	Schwartz, J. P., Pearson, J. & Johnson, E. M. Brain Res. 244, 378−381 (1982). | Article | PubMed | ISI | ChemPort |
8.	Rich, K. M., Yip, H. K., Osborne, P. A., Schmidt, R. E. & Johnson, E. M. J. comp. Neurol. 230, 110−118 (1984). | PubMed | ISI | ChemPort |
9.	Levi-Montalcini, R. & Angeletti, P. U. Physiol. Rev. 48, 534−569 (1968). | PubMed | ChemPort |
10.	Thoenen, H. & Barde, Y. A. Physiol. Rev. 60, 1284−1335 (1980). | PubMed | ISI | ChemPort |
11.	Hinsey, J. C., Krupp, M. A. & Lhamon, W T. J. comp. Neurol. 67, 205−214 (1937).
12.	Hare, W. K. & Hinsey, J. C. J. comp. Neurol. 73, 489−502 (1940).
13.	Yip, H. K. & Johnson, E. M. Proc. natn. Acad. Sci. U.S.A. 81, 6245−6249 (1984). | ChemPort |
14.	Richardson, P. M. & Riopelle, R. J. J. Neurosci. 4, 1683−1689 (1984). | PubMed | ISI | ChemPort |
15.	Coggeshall, R. E. Neurosurgery 4, 443−448 (1979). | PubMed | ISI | ChemPort |
16.	Snedecor, G. W. in Statistical Methods (Iowa University Press, 1957).
17.	Konigsmark, B. E. in Contemporary Research Methods in Neuroanatomy (eds Nauta, W. H. & Ebbesson, S. O. E.) 315−340(Springer, New York, 1970).