Abstract
The role of nerve growth factor (NGF) in the development of embryonic sympathetic neurons was examined in vivo. Individual mouse embryos received transuterine injections of NGF or antiserum to NGF (anti-NGF), and the effects on the superior cervical ganglion (SCG) were studied. Treatment with NGF at any gestational stage, from the time of ganglion aggregation to birth, increased ganglion tyrosine hydroxylase (T-OH) activity. Both the number of catecholaminergic neurons and T-OH activity per neuron were increased. Choline acetyltransferase (ChAc) activity was increased by NGF at early gestational stages, but not at later stages. These observations suggest that perikarya containing ChAc are responsive to NGF, whereas preganglionic nerve terminals are not. Treatment with anti-NGF rapidly and permanently decreased ganglion T-OH activity. The effects of anti-NGF were more pronounced at later gestational stages, suggesting that ganglia become increasingly dependent on NGF during development. Alteration of maternal levels of NGF had no effect on development of the embryonic SCG, suggesting that local embryonic concentrations of NGF are responsible for modulating sympathetic ontogeny.
Original language | English (US) |
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Pages (from-to) | 157-168 |
Number of pages | 12 |
Journal | Brain research |
Volume | 189 |
Issue number | 1 |
DOIs | |
State | Published - May 5 1980 |
Funding
This work was supported by NIH Grants HD 12108 and NS 10259 and aided by grants from the Dysautonomia Foundation Inc. and the National Foundation--March of Dimes. J.A.K. is the recipient of Teacher Investigator Award NS 00351. I.B.B. is the recipient of the Irma T. Hirschl Career Scientist Award.
Keywords
- acetyltransferase
- choline
- development
- nerve growth factor
- sympathetic neurons
- tissue culture
- tyrosine hydroxylase
ASJC Scopus subject areas
- General Neuroscience
- Molecular Biology
- Clinical Neurology
- Developmental Biology