Trans-synaptic regulation of tyrosine hydroxylase activity in a developing mouse sympathetic ganglion: Effects of nerve growth factor (NGF), NGF-antiserum and pempidine

Abstract

The response of the normal and surgically decentralized mouse superior cervical ganglion to nerve growth factor (NGF) and its antiserum have been studied in neonatal animals. NGF was able to increase the activity of the enzyme tyrosine hydroxylase, used as a marker for adrenergic neurones, in both normal and decentralized ganglia. However, it was unable to reverse the acute effects of surgical decentralization; a significant difference in tyrosine hydroxylase activity between the control and decentralized ganglia was observed even after the NGF treatment. In addition, 7 weeks after the NGF treatment had ceased, the enzyme activity returned to levels not significantly different from those in animals that had never received NGF. NGF antiserum was equally effective in causing a reduction in tyrosine hydroxylase activity in normal and decentralized ganglia. The ganglion blocking drug pempidine when administered to neonatal mice mimicked the effects of surgical decentralization; tyrosine hydroxylase activity of the superior cervical ganglia of animals treated with this drug failed to develop normally. It was also found that, as in surgically decentralized animals, NGF was unable to reverse the effects of pempidine. The effects of NGF were transient, while the effects of decentralization and pempidine were long lasting, suggesting that the most important regulation for ganglion development is the influence of trans-synaptic activity, most probably mediated by the depolarizing action of acetylcholine.