Nerve Terminals In Sympathetic Ganglia Research Articles

Exocytotic release from neuronal cell bodies, dendrites and nerve terminals in sympathetic ganglia of the rat, and its differential regulation

Stimulant-induced exocytosis has been demonstrated in sympathetic ganglia of the rat by in vitro incubation of excised ganglia in the presence of tannic acid, which stabilizes vesicle cores after their exocytotic release. Sites of exocytosis were observed along non-synaptic regions of the surfaces of neuron somata and dendrites, including regions of dendrosomatic and dendrodendritic apposition, as well as along the surfaces of nerve terminals. About half the exocytoses associated with nerve terminals were parasynaptic or synaptic, and these appeared mostly to arise from the presynaptic terminal, but occasionally from the postsynaptic element. The results demonstrated that the neurons of sympathetic ganglia release materials intraganglionically in response to stimulation, that release from different parts of the neuron is subject to independent regulation, at least via cholinergic receptors, and that release is partly diffuse, potentially mediating autocrine or paracrine effects, and partly targeted toward other neurons, but that the latter mode is not necessarily, and not evidently, synaptic. Specifically, exocytosis from all locations increased significantly during incubation in modified Krebs' solution containing 56 mM potassium. Observation of the effects of cholinergic agonists (nicotine, carbachol, oxotremorine) and antagonists (atropine, AF-DX 116) showed that nicotinic and muscarinic excitation each, independently, increased the incidence of exocytosis from somata and dendrites. Exocytosis from nerve endings was not altered by nicotine, but was enhanced or, at high initial rates of exocytosis, decreased, by muscarinic stimulation. Evidence was obtained for muscarinic auto-inhibition of exocytosis from nerve terminals, occurring under basal incubation conditions, and for a muscarinic excitatory component of somatic exocytosis, elicitable by endogenous acetylcholine. The M 2-selective muscarinic antagonist AF-DX 116 was found to modify the exocytotic response of the dendrites to oxotremorine, widening the range of its variation; this effect is consistent with recent evidence for the presence of M 2-like muscarinic binding sites, in addition to M 1-like binding, upon these dendrites. [88] Over all conditions, disproportionately more sites of somatic and dendritic exocytosis were found to be located in regions of dendrosomatic and dendrodendritic apposition than would be expected from the relative extent of the neuronal surface occupied by these relationships. Such mechanisms of intraganglionic release may be expected to contribute to the regulation and integration of the behaviour of the various functionally distinctive populations of neurons in these ganglia, by autocrine, paracrine, and focal, neuroneuronal, routes of action. Similar phenomena of exocytotic somadendritic release might prove to subserve integrative neuroneuronal interactions more widely throughout the nervous system.

Effects of atropine on nicotinic transmission in bullfrog sympathetic ganglia.

Effects of atropine on nicotinic transmission in bullfrog sympathetic ganglia were examined by the intracellular microelectrode technique. The fast excitatory postsynaptic potential (fast EPSP) of ganglion cells recorded in Ca2+ -deficient solution is depressed in the presence of atropine (3-30μM). The mean amplitude of fast EPSP is decreased to about 60% of normal with 30μM atropine. The quantal content calculated from these fast EPSPs by the variance method increases in the presence of atropine to 160% of normal with 30μM atropine. The amplitude of fast ACh-potential decreases to about 30% of normal, and that of miniature EPSPs decreases to about 35% of normal in the presence of atropine (30μM). Thus, it seems that atropine facilitates the evoked release of ACh from preganglionic nerve terminals in sympathetic ganglia.

Enkephalin‐like immunoreactivity in nerve terminals in sympathetic ganglia and adrenal medulla and in adrenal medullary gland cells

Enkephalin‐like immunoreactivity in nerve terminals in sympathetic ganglia and adrenal medulla and in adrenal medullary gland cells

Evidence for adrenergic nerve terminals and synapses in sympathetic ganglia

Histochemical evidence has been presented that a monoamine, probably norepinephrine, is located in nerve terminals in sympathetic ganglia of the cat. These terminals were found between and around the ganglion cells, forming structures highly suggestive of synapses. They are probably adrenergic synaptic nerve terminals.