IMPAIRED MATURATION OF PRE-SYNAPTIC CHOLINERGIC NERVE TERMINALS IN THE SUPERIOR CERVICAL GANGLIA AFTER ADMINISTRATION OF GUANETHIDINE AND DEXAMETHASONE

Abstract

The role of postsynaptic cells in development of pre-synaptic cholinergic nerve terminals was investigated in immature rat superior cervical ganglia (SCG) and adrenals employing chemical agents which prevent normal maturation of postsynaptic cells. A marked atrophy of ganglion adrenergic neurons after guanethidine administration was accompanied by complete failure of normal maturation of choline acetyltransferase (ChAc) activity in presynaptic endings. The same treatment failed to alter levels of ChAc in mature ganglia despite the marked atrophy of adrenergic neurons. Administration of dexamethasone resulted in a growth retardation of ganglion neurons and adrenal chromaffin cells reflected by lower levels of tyrosine hydroxylase and dopamine-.beta.-hydroxylase than those in untreated tissues. Levels of ChAc were significantly lower in the ganglia, but not in adrenals when treatment was started immediately after birth. Apparently normal synapse formation in the SCG depends on normal maturation of adrenergic neurons, and this dependence is detectale only during a limited period of life.