Stimulant-induced exocytosis from neuronal somata, dendrites, and newly formed synaptic nerve terminals in chronically decentralized sympathetic ganglia of the rat.

Loss of preganglionic neurones underlies the autonomic failure of human multiple system atrophy. In rat sympathetic ganglia decentralization leads to new synapse formation. We explored whether these synapses are functional, and whether chronically decentralized neurones respond normally to activation, in terms of exocytosis. Potassium depolarization and cholinergic agonists were applied to freshly excised rat superior cervical sympathetic ganglia, preganglionically denervated with prevented reinnervation 5 months earlier. Ganglia were incubated and stimulated in the presence of tannic acid, which stabilizes released vesicle cores for subsequent electron microscopy. In denervated ganglia exocytosis was observed from newly formed synaptic nerve terminals, and from nonsynaptic surfaces of neurone somata and dendrites. The results demonstrated that the new intraganglionic synapses, which are mostly catecholaminergic, can function and that chronically decentralized sympathetic neurones remain capable of stimulant-induced exocytosis from somata and dendrites. The maximal release upon potassium depolarization did not differ significantly between denervated and contralateral ganglia. Relative to this, the exocytotic responses of decentralized somata and dendrites to nicotine resembled those of contralateral ganglia. Responses to muscarine were significantly less in denervated than in contralateral ganglia, indicating inhibition in dendrites. Responses to carbachol suggested interactions between nicotinic and excitatory muscarinic effects. Nerve terminals in denervated ganglia showed high basal release. Their responses to muscarine and carbachol resembled those of the decentralized neurones, from which most may originate. Their response to nicotine evidenced inhibition. Their actions, coupled with nonsynaptic effects of soma-dendritic exocytosis, might modulate responses of the decentralized neurone population to other surviving inputs. This modulation could be influential in disease-induced decentralization in man.