Release of acetylcholine at voluntary motor nerve endings

Dale, H. H.; Feldberg, W.; Vogt, Marthe

doi:10.1113/jphysiol.1936.sp003371

Cited by 439 publications

(99 citation statements)

References 9 publications

(4 reference statements)

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“…This release takes place only in presence of physostigmine, but this is a condition prevailing also at the junction. In fact, it was emphasized by Dale and his associates that ACh appears in the perfusion fluid of junctions only in presence of physostigmine (24). Since physostigmine is a powerful inhibitor of ACh-esterase, the necessity of blocking the extremely rapid physiological removal mechanism in order to obtain an extracellular appearance raises the question whether this appearance takes place physiologically, i.e., with the enzyme at full activity.…”

Section: Discussionmentioning

confidence: 99%

Effect of Ions on the Efflux of Acetylcholine from Peripheral Nerve

Dettbarn

Rosenberg

1966

The Journal of General Physiology

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The nerves from the walking leg of lobster released acetylcholine (ACh) even when the ends were tied off, although this release was significantly increased when the nerve endings were not tied. The resting nerves were kept in sea water containing physostigmine. In absence of physostigmine no ACh was found in the surrounding fluid. Removal of Ca from the sea water reduced the release of ACh, while increased concentrations of Ca had no significant effect. Removal of Mg++ or increased Mg++ concentrations in the presence of normal Ca + + concentrations increased the release of ACh. Increased K+ concentrations had a stimulating action on the efflux of ACh. Increased or reduced Na+ concentrations had only slight effects on the release of ACh in resting lobster nerve. During the 4 hr observation period the excised nerves were still able to synthesize ACh. The choline acetylase activity was stimulated by increased concentrations of Mg + + and K+. The effects of ions on the release of ACh are similar to those reported at the junction.

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Section: Discussionmentioning

confidence: 99%

Effect of Ions on the Efflux of Acetylcholine from Peripheral Nerve

Dettbarn

Rosenberg

1966

The Journal of General Physiology

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“…This subsequently was understood to mean that curare alkaloids had only a post--junctional action, and did not change the amount of transmitter released by a nerve impulse, although Dale et al (1936) did not make such a categorical statement and their methods of estimation of acetylcholine were not precise enough to do so. Lilleheil & Naess (1961) concluded that tubocurarine (Tc) in addition to its postjunctional effect also haid a pre-junctional action which was responsible for the rapid decline of the end-plate potential (e.p.p.)…”

Section: Introductionmentioning

confidence: 99%

The prejunctional actions of some non‐depolarizing blocking drugs

Blaber

1973

British J Pharmacology

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3. Tubocurarine and benzoquinonium depressed the rate of refilling of the available store causing its depletion at high rates of stimulation. This was offset by an increase in fractional release, which in the case of tubocurarine was sufficient for the quantal content of the first e.p.p. to be unchanged. 4. Dimethyltubocurarine and pancuronium had a similar effect to tubocurarine on the rate of refilling of the store and depletion of the store at high rates of stimulation but did not increase fractional release. There was, therefore, a decrease in the quantal content of the first e.p.p. 5. Lignocaine depressed the rate of refilling of the store and depleted the store at high rates of stimulation. Fractional release was also depressed.6. It is suggested that the non-depolarizing drugs have a weak local anaesthetic action retarding the influx of sodium into the nerve terminal which slows the rate of refilling of the store. This effect is due to the quaternary ammonium head. The presence of a phenolic group increases fractional release due either to an increased influx of calcium into the nerve terminal or to a potentiation of the actions of calcium.

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“…Dale et al (1936) found that the amount of ACh released into the solution perfusing striated muscle was not diminished when the muscles were completely paralysed by curare. They concluded that curare had principally a postjunctional action.…”

Section: Stimulationmentioning

confidence: 94%