The efferent sympathetic fibers which leave the central nervous system in connection with certain of the cranial and spinal nerves all end in sympathetic ganglia and are known as preganglionic fibers. ❋ Unknown (1918)
The cells of this column are fusiform or star-shaped, and of a medium size: the axons of some of them pass into the anterior nerve roots, by which they are carried to the sympathetic nerves: they constitute the white rami and are sympathetic or visceral efferent fibers; they are also known as preganglionic fibers of the sympathetic system; the axons of others pass into the anterior and lateral funiculi, where they become longitudinal. ❋ Unknown (1918)
We have evidence, then, that both the reserve of acetylcholine, and the esterase required for its destruction, are in fact associated with the preganglionic nerve endings, as our hypothesis demands. ❋ Unknown (1965)
Feldberg and Gaddum17, though unable to reproduce effects obtained by Kibjakow with pure Locke's solution, found that, when eserine was added to the fluid perfusing the ganglion, stimulation of the preganglionic fibres regularly caused the appearance of acetycholine in the venous effluent. ❋ Unknown (1965)
The first is a depot, closely related to the preganglionic or motor nerve ending12, in which acetylcholine may be held in some association which prevents its action and protects it from destruction, and from which it can be immediately liberated by the arrival of a nerve impulse. ❋ Unknown (1965)
Feldberg13, in my laboratory, have obtained evidence that nearly the whole of the acetylcholine, obtainable by extraction from a normal sympathetic ganglion, disappears when the preganglionic nerve fibres are caused to degenerate by section; so that its maintenance is, in fact, dependent on the integrity of the preganglionic nerve endings. ❋ Unknown (1965)
In elegant experiments directed towards the question of the localization of the release of Ac.Ch. in the ganglion, Feldberg and Vartiainen24 were recently able to prove that it was released neither by the preganglionic fibres nor by the ganglion cells themselves, the only direct effector organ. ❋ Unknown (1965)
If, therefore, it can be proved that Ac.Ch. is formed in the "synapse", it can only, in my opinion, be in the preganglionic nerve ending or in the ganglion cell. ❋ Unknown (1965)
Gaddum23 have shown that stimulation of the preganglionic sympathetic fibres in the neck releases Ac.Ch. in the sup.cerv. ganglion, which itself stimulates the ganglion, so that progressive stimulation is set up in the postganglionic fibres. ❋ Unknown (1965)
In a sympathetic ganglion, the synaptic junctions, at which the acetylcholine is released by the incident preganglionic impulses, form a large part of the small amount of tissue perfused. ❋ Unknown (1965)
It was clear that, if the liberation took place actually at the synapses, the acetylcholine liberated by each preganglionic impulse, in small dose, indeed, but in much higher concentration than that in which it reached the venous effluent, must act as a stimulus to the corresponding ganglion cells. ❋ Unknown (1965)
If, by calculation, we estimate the amount of acetylcholine thus obtained from the effect of a single motor impulse, arriving at a single nerve ending, the quantity is of the same order as that similarly estimated for a single preganglionic impulse and a single ganglion cell; in both cases ❋ Unknown (1965)
Even when obtained in solution this potent enzyme destroys acetylcholine with a quite remarkable rapidity; and if we could suppose it to be concentrated on surfaces at preganglionic or motor nerve endings, in immediate relation to the site of liberation and action of acetylcholine, it might furnish an adequate mechanism for the complete destruction of this substance, even during the very brief interval of the refractory period. ❋ Unknown (1965)
We must suppose that an impulse, arriving at the ending of a preganglionic or a voluntary motor nerve fibre, releases with a flashlike suddenness a small charge of acetylcholine, in immediate contact with the ganglion cell or the motor end plate of the muscle fibre. ❋ Unknown (1965)
They showed, further, that the ganglion cells might be paralysed by nicotine or curarine, so that they would no longer respond to preganglionic stimulation or to the injection of acetylcholine, but that such treatment did not, in the least, diminish the output of acetylcholine caused by the arrival of preganglionic impulses at the synapses. ❋ Unknown (1965)
Although proof of this has so far only been obtained directly in the case of preganglionic sympathetic endings, there is, nevertheless, much to make us think that in other places as well the nerve substances are released in the nerve endings themselves. ❋ Unknown (1965)
In both cases, the phenomenon had the appearance of a direct, unbroken conduction, to ganglion cell or muscle fibre, of the same propagated wave of physico-chemical disturbance as had constituted the preganglionic or the motor nerve impulse, with only a slight, almost negligible retardation in its passage across the ganglionic synapse or the neuromuscular junction. ❋ Unknown (1965)
Feldberg and Vartiainen18 then showed that it was, in fact, only the arrival of preganglionic impulses at synapses which caused the acerylcholine to appear. ❋ Unknown (1965)
The parasympathetic nerve fibers, on the contrary, travel to ganglia within the organ they are aiming at; as a result, the preganglionic fibers are quite long and the postganglionic fibers very short. ❋ Asimov, Isaac (1963)
The preganglionic fibers of the sympathetic division end at the sympathetic trunks or at the prevertebral ganglia, so these fibers are quite short. ❋ Asimov, Isaac (1963)
