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Biomedical subjects

H Thoenen

Publications and source records attributed to H Thoenen.

At least 253 records · Page 14Linked to original sources
PubMed1974

The retrograde axonal transport of nerve growth factor.

A retrograde axonal transport of nerve growth factor (NGF) from the adrenergic nerve terminals in the mouse iris to the cell bodies of postganglionic sympathetic neurones in the superior cervical ganglion has been demonstrated. After injection of iodinated nerve growth factor (125I-NGF) into the anterior eye-chamber there was a relatively rapid accumulation of radioactivity in the superior cervical ganglia on both injected and non-injected sides, as was the case after subcutaneous injection. However, 4 h after intraocular injection a preferential accumulation of radioactivity became apparent in the superior cervical ganglion on the injected side, and this difference between the ganglia on injected and non-injected sides gradually increased to a maximum at 16 h. Transection of the postganglionic adrenergic fibres as well as the prior intraocular injection of colchicine abolished the preferential accumulation of 125I-NGF in the superior cervical ganglion of the injected side, whereas the destruction of adrenergic nerve terminals by 6-hydroxydopamine did not impair the preferential accumulation. It is concluded that the retrograde axonal transport of NGF, which was estimated to take place at a rate of about 2.5 mm/h, depends on a colchicine-sensitive mechanism as does the orthograde rapid axonal transport. However, the uptake of NGF may not only take place from the nerve terminals but also from the preterminal parts, as has been shown in other studies with horseradish peroxidase. Autoradiographic studies strongly supported the existence of a retrograde transport by showing a clear localization of radioactivity in a small number of neurones in the superior cervical ganglion on the injected side, whereas on the non-injected side there was only a diffuse distribution of radioactivity throughout the ganglion.

Animals↗
PubMed1974

Location of an isoproterenol-responsive cyclic AMP pool in adrenergic nerve cell bodies and its relationship to tyrosine 3-monooxygenase induction.

To decide whether adenosine 3':5'-cyclic monophosphate (cyclic AMP) plays a role as a second messenger in the trans-synaptic induction of tyrosine 3-monooxygenase (EC 1.14.16.2), it is desirable to discriminate between neuronal and extraneuronal changes in cyclic AMP concentration. Treatment of newborn rats with nerve growth factor antiserum or 6-hydroxydopamine, leading to destruction of 61-85% of the adrenergic nerve cell bodies in the superior cervical ganglion, led to a decrease in cyclic AMP of only 16-28%. This observation demonstrates that a relatively small portion of cyclic AMP is localized in the adrenergic neurons. However, administration of isoproterenol produced an increase (12-fold) in cyclic AMP only in this neuronal pool. Neither single nor repeated injections of isoproterenol led to induction of tyrosine monoxygenase. This, together with previous observations that experimental conditions leading to induction of the enzyme do not produce significant increases of cyclic AMP in the whole ganglion, is taken as an indication that cyclic AMP is not acting as a second messenger in the trans-synaptic induction of tyrosine monooxygenase in the rat superior cervical ganglion. In the rat adrenal medulla, treatment with reserpine led to both a shortlasting (60-90 min) increase in cyclic AMP and a subsequent induction of tyrosine monooxygenase. However, the increase in cyclic AMP was almost completely prevented (40 compared to 320%) by pretreatment of the rats with propranolol while the induction of tyrosine monooxygenase was not diminished. This observation also argues against an exclusive key-function of cyclic AMP in trans-synaptic induction of tyrosine monooxygenase in the adrenal medulla.

Adrenal Medulla↗