The effect of acetylcholine upon mammalian motor nerve terminals.

Hubbard, J. I.; Schmidt, Robert F.; Yokota, Toshikatsu

doi:10.1113/jphysiol.1965.sp007799

Cited by 125 publications

(56 citation statements)

References 40 publications

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“…It has been reported that the quantal content of end-plate potentials is reduced in the presence of ACh (Ciani & Edwards, 1963;Hubbard et al 1965). Similar observations were obtained with bullfrog sympathetic ganglia in our recent studies.…”

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confidence: 91%

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Cholinergic receptors at sympathetic preganglionic nerve terminals

Koketsu¹,

Nishi²

1968

The Journal of Physiology

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SUMMARY1. In the paravertebral sympathetic chain of bullfrogs, some part of the preganglionic nerve located within the ganglion was depolarized transiently when acetylcholine (ACh) was directly applied to the ganglion, particularly in the presence of an anticholinesterase (anti-ChE). The axonal part of the preganglionic nerve, on the other hand, showed no detectable depolarization following direct application of ACh (with anti-ChEs) to the interganglionic nerve trunk.2. The ACh depolarization was markedly depressed by nicotine, and less markedly by (+ )-tubocurarine, whereas it was not affected by atropine. Nicotine, similar to ACh, transiently depolarized only the intraganglionic portion of the presynaptic fibres.3. The action potentials, recorded from the axonal as well as the terminal parts of the preganglionic nerve, showed spike potentials followed by a marked negative after-potential. The negative after-potential was followed by a positive after-potential which was markedly enhanced by repetitive nerve stimulation.4. A slow negative potential followed the positive after-potential in the repetitive responses of the terminal parts of the preganglionic nerve. The slow negative potential was enhanced by anti-ChEs, eliminated by ACh and nicotine, and unaffected by atropine.5. The amplitude of the action potentials of the terminal parts of the preganglionic nerve, and particularly that of the negative after-potential, was significantly depressed during the development of ACh depolarization as well as the slow negative potential, indicating that the two types of slow depolarization originated in the intraganglionic portion of the presynaptic fibres, presumably somewhere near or at the nerve terminals.6. ACh depolarization similar to that observed with bullfrog sympathetic ganglia was observed with rat superior cervical ganglia. The present K. KOKETSU AND S. NISHI experiments provide evidence that a certain part of the preganglionic nerve terminals is depolarized by the action of the transmitter released from their endings.

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“…It may be the membrane of the nerve terminal endings (cf. Volle & Koelle, 1961;Koelle & Koelle, 1959; Koelle, 1961Koelle, , 1962 or the membrane of a more proximal part of the preganglionic nerve terminals (Hubbard, Schmidt & Yokota, 1965). In any case,…”

Section: Discussionmentioning

confidence: 98%

Cholinergic receptors at sympathetic preganglionic nerve terminals

Koketsu¹,

Nishi²

1968

The Journal of Physiology

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“…This finding is difficult to reconcile with the proposed cholinergic recurrent excitatory pathway to motoneurones (Matsurra, 1971), although it is conceivable that recording from the spinal roots might not have detected small responses generated in the motoneurone dendrites. The fact that unmyelinated nerve terminals of the primary afferents are unresponsive to acetylcholine and carbachol suggests that the acetylcholine sensitivity observed in some unmyelinated fibres and terminals (Armett & Ritchie, 1960;Hubbard, Schmidt & Yokota, 1965;Koketsu & Nishi, 1968) does not apply to all nerve fibres.…”

Section: Discussionmentioning

confidence: 99%

THE ACTION OF ACETYLCHOLINE ANTAGONISTS ON AMINO ACID RESPONSES IN THE FROG SPINAL CORD in vitro

NICOLL

1975

British J Pharmacology

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I The isolated hemisected frog spinal cord has been used to study the action of acetylcholine antagonists on amino acid responses by means of sucrose gap recording. 2 Primary afferents and motoneurones were shown to contain few, if any, cholinoceptors, since acetylcholine and carbachol responses were essentially abolished when synaptic transmission was blocked with magnesium ions or when action potentials were blocked by tetrodotoxin.3 Curare antagonized the y-aminobutyric acid (GABA) and ,B-alanine depolarizations of primary afferents and the hyperpolarizing action of these amino acids on motoneurones. Nicotine also antagonized 3-alanine depolarizations and to a small extent GABA depolarizations of primary afferents. These actions are similar to but weaker than those obtained previously with picrotoxin. 4 Atropine selectively antagonized 3-alanine depolarizations of primary afferents and blocked ,B-alanine and glycine hyperpolarizations of motoneurones. GABA responses were entirely resistant to the action of atropine. These actions are similar to but 50 times weaker than those obtained previously with strychnine. 5 Dihydro-,B-erythroidine, tetraethylammonium, and gallamine were entirely ineffective in antagonizing amino acid responses. Since these agents are known to block the dorsal root potential elicited by ventral root stimulation but have no effect on the amino acid responses of primary afferents, it is evident that a cholinergic step is involved in this pathway.

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“…Increased magnesium concentration An excess concentration of magnesium ions impairs neuromuscular transmission in two ways: it decreases transmitter release from motor nerve endings (del Castillo & Engbaeck, 1954;Dodge & Rahamimoff, 1967) and it stabilizes the postjunotional membrane, thereby depressing its excitability (Engbaeck, 1947;del Castillo & Engbaeck, 1954). Magnesium ions also prevent the depolarization of motor nerve terminals produced by acetylcholine (Hubbard, Schmidt & Yokota, 1965).…”

Section: Resultsmentioning

confidence: 99%

Actions of acetylcholine and carbachol on the chick biventer cervicis muscle

Marshall

1971

British J Pharmacology

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Summary1. The possibility that carbachol may act on the chick biventer cervicis muscle by releasing acetylcholine was investigated. 2. Log dose-response curves for acetylcholine and carbachol were constructed in the presence of triethylcholine, tubocurarine and physostigmine, in both innervated and denervated chick biventer cervicis muscles. 3. The log dose-response curve for acetylcholine -was shallower than that for carbachol and was moved to the left by triethylcholine, indicating potentiation.In the presence of physostigmine, the curve was as steep as that for carbachol, and like that for carbachol was moved to the right by triethylcholine, indicating antagonism. In the presence of tubocurarine, the log dose-response curves for both acetylcholine and carbachol were moved to the right. 4. The log dose-response curves for both acetylcholine and carbachol were moved to the left by chronic denervation, indicating increased sensitivity to these drugs. Both curves were moved similar distances to the right by excess magnesium ion concentration. No tachyphylaxis developed to repeated administration of carbachol in the presence of triethylcholine or tubocurarine, either in innervated or denervated muscles. 5. It was concluded that the main action of triethylcholine in the chick biventer cervicis muscle is a tubocurarine-like action, which, in the presence of acetylcholine, is masked by a weak anticholinesterase action. It was also concluded that the diminished response to carbachol in the presence of triethylcholine is due to the postjunctional blocking action of triethylcholine. and that carbachol owes none of its activity to an ability to release acetylcholine from the nerve terminals.

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The effect of acetylcholine upon mammalian motor nerve terminals.

Cited by 125 publications

References 40 publications

Cholinergic receptors at sympathetic preganglionic nerve terminals

Cholinergic receptors at sympathetic preganglionic nerve terminals

THE ACTION OF ACETYLCHOLINE ANTAGONISTS ON AMINO ACID RESPONSES IN THE FROG SPINAL CORD in vitro

Actions of acetylcholine and carbachol on the chick biventer cervicis muscle

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