Facilitation by stannous chloride of transmitter release from motor nerve terminals

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Enhancement by carbachol of transmitter release from motor nerve terminals.

In the endplates of rat phrenic nerve-diaphragm, application of the acetylcholine-like compound, carbachol, causes a marked increase in transmitter release, as measured electrophysiologically using miniature endplate potential frequency. Washing out of carbachol reverses the increase in frequency. The ability of carbachol to increase transmitter release is greatly enhanced by perfusion of the p...

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Calcium and transmitter release at nerve terminals.

Dolphin, A. C. and Scott, R. H. (1987) J. Physiol. (London) 386, 1-17 Holz, G. G., Rane, S. G. and Dunlap, K. (1986) Nature (London) 319,670-672 Scott, R. H. and Dolphin, A. C. (1986) Neurosci. Lett. 69,59-64 Lewis, D. L., Weight, F. F. and Luini, A. (1986) Proc. Natl. Acad. Sci. U.S.A. 83, 9035-9039 Grassi, F. and Lux, H. D. (1989) Neurosci. Lett. 105, 113-1 19 Dolphin, A. C., Huston, E. and S...

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Dual effects of theophylline on spontaneous transmitter release from frog motor nerve terminals.

Alkylxanthine drugs, such as theophylline, block adenosine receptors, inhibit phosphodiesterases and other enzymes, and cause the release of calcium from intracellular stores. Adenosine receptor blockade occurs at low micromolar concentrations of the drugs, while other effects occur in the millimolar concentration range. The effects of theophylline were tested on spontaneous transmitter release...

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Adenosine depresses spontaneous transmitter release from frog motor nerve terminals by acting at an A1-like receptor.

Adenosine (1 microM to 1 mM) depressed spontaneous transmitter release from frog motor nerve terminals without producing any observable postsynaptic effects. Since this action of adenosine was blocked by 20 microM theophylline and 1 microM 8-phenyltheophylline, adenosine probably acts at a specific receptor on motor nerve terminals to reduce spontaneous transmitter output. The effects of the ad...

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Mefloquine selectively increases asynchronous acetylcholine release from motor nerve terminals.

Effectiveness against chloroquine-resistant Plasmodia makes mefloquine a widely used antimalarial drug. However, mefloquine's neurologic effects offset this therapeutic advantage. Cellular actions which might contribute to the neurologic effects of mefloquine are not understood. Structural similarity to tacrine suggested that mefloquine might alter cholinergic synaptic transmission. Therefore, ...

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ژورنال

عنوان ژورنال: Japanese Journal of Pharmacology

سال: 1989

ISSN: 0021-5198

DOI: 10.1016/s0021-5198(19)56673-2