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4 edition of Mechanism of [alpha]-latrotoxin action at the frog neuromuscular junction found in the catalog.

Mechanism of [alpha]-latrotoxin action at the frog neuromuscular junction

Chris Tsang

Mechanism of [alpha]-latrotoxin action at the frog neuromuscular junction

by Chris Tsang

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  • 30 Currently reading

Published by National Library of Canada in Ottawa .
Written in English


Edition Notes

Thesis (M.Sc.) -- University of Toronto, 2000.

SeriesCanadian theses = -- Thèses canadiennes
The Physical Object
FormatMicroform
Pagination1 microfiche : negative. --
ID Numbers
Open LibraryOL20412010M
ISBN 100612504638
OCLC/WorldCa51838222

Pincus, Yaari and Argov, Antiepileptic Drugs: Mechanisms of Action (), evaluating the effects of PHT on calcium flux at the frog neuromuscular junction, found that PHT ( µM), in normal calcium medium, reduced quantal content and endplate potential amplitude. In low calcium medium, however, PHT increased quantal content and endplate. Calcium-dependent presynaptic action of substance P at the frog neuromuscular junction. Steinacker, A. Nature () [ Pubmed ] Lithium reduces the number of acetylcholine receptors in skeletal muscle.

(). Voltage clamp analysis of acetylcholine induced end-plate current fluctuations at frog neuromuscular junction. (). Voltage-dependence of drug-induced conductance in frog neuromuscular junction. (). Voltage-dependent ffect of curare at the frog neuromuscular by:   Mechanisms of the inhibition of evoked multiquantal endplate currents (EPC) by chlorhexidine (CHX) were studied in electrophysiological experiments and by mathematical modeling to discriminate between possible channel, receptor, and non-receptor effects of this common antiseptic drug. Experiments were carried out on the isolated neuromuscular preparation of the cut m. sartorius of the frog.

Discuss the underlying Mechanisms of insulin synthesis - Biology bibliographies - in Harvard style. Change style These are the sources and citations used to research Discuss the underlying Mechanisms of insulin synthesis. TURNOVER OF TRANSMITTER AND SYNAPTIC VESICLES AT THE FROG NEUROMUSCULAR JUNCTION - The Journal of Cell Biology.   Evoked transmitter release increased by inorganic mercury at frog neuromuscular junction. Evaluation of the effects and mechanisms of action of mercuric chloride on striatal dopamine release Cited by:


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Mechanism of [alpha]-latrotoxin action at the frog neuromuscular junction by Chris Tsang Download PDF EPUB FB2

The neuromuscular junction is the chemical synapse between motor neurons and skeletal muscle fibers. It is designed to reliably convert the action potential from the presynaptic motor neuron into the contraction of the postsynaptic muscle by: Mechanisms of ATP action on motor nerve terminals at the frog neuromuscular junction Article in European Journal of Neuroscience 21(5) April with 12 Reads How we measure 'reads'.

Drugs and toxins are known that interrupt neuromuscular transmission by an action on the nerve endings through which acetylcholine synthesis, storage or release is impaired. Important examples are hemicholinium-3, which inhibits acetylcholine synthesis, and the exotoxin of Clostridium botulinum, which interferes with the transmitter release Author: W.

Bowman. Calmodulin Inhibitors and Transmitter Release at the Frog Neuromuscular Junction.- Studies on the Mechanism of the Inhibitory Action of Verapamil on Ca2+ Transport.- Manganese and Asynchronous Transmitter Release at the Frog Neuromuscular Junction.- Several Potassium Conductances Modulate the Excitability of Frog Motor Nerve Terminals Purchase Neurotransmitter Release the Neuromuscular Junction - 1st Edition.

Print Book & E-Book. ISBNThe frog neuromuscular junction has played a central role in understanding synaptic mechanisms. It has served as the primary model system in which to study the processes by which information is transmitted from an axon terminal to a post-junctional cell.

action potential in the plasma membrane of the muscle fiber leads to force production via an increase in intracellular calcium and crossbridge formation and turn-over.

Excitation begins at the neuromuscular junction and then the action potential spreads over the surface membrane and inward into the fiber via the transverse tubule system. the action of trypsin on blockade by 2‐halogenoalkylamines: speculation on the nature of the alpha receptor for catecholamine.

graham; h. al katib; pages: ; first published: october 7: Betz WJ, Bewick GS. Optical analysis of synaptic vesicle recycling at the frog neuromuscular junction. Science. Jan 10;() PMID: 8: Wood SJ, Slater CR. The contribution of postsynaptic folds to the safety factor for neuromuscular transmission in rat fast- and slow-twitch muscles.

J Physiol. Apr 1; (Pt 1. Transmitter release at the frog neuromuscular junction was studied after sodium influx in nerve and muscle was abolished by tetrodotoxin (TTX). In the presence of TTX, transmitter release evoked by electrotonic depolarization of the nerve terminal was potentiated following presynaptic stimulation by a train of depolarizing by:   This pharmacology lecture covers topics such as mechanism of action of cholinergic antagonists; antimuscarinic agents, ganglionic blockers, neuromuscular nondepolarizing &.

Brain Research, () Elsevier Biomedical Press The Effect of Streptomycin on the Neuromuscular Junction of the Frog MITSUYUKI TAMAKI Institute of Clinical Medicine, The University of Tsukuba, Niihari-gun, Ibaraki-ken, (Japan) (Accepted September 2lst, ) Key words: streptomycin -- neuromuscular junction -- frog The neuromuscular block produced by Cited by: 1.

Mechanisms of the Effect of Dimephosphone on Synaptic Transmission in the Frog Neuromuscular Junction Article in Neurophysiology 34(5) September. In order to realize the mechanism of neurotoxin in snake venom, first we have to know what happens in the normal neuromascular junction.

The neuromuscular junction contains the membrane of the axon terminal of the motor neuron, also called presynaptic membrane, or presynaptic site; the motor end-plate of muscle cell, also called postsynaptic. The mechanisms of action of phorbol ester and diacylglycerol are discussed in relation to the control of acetylcholine release and action at the neuromuscular junction.

Full text Get a printable copy (PDF file) of the complete article (M), or click on a page image below to browse page by page. Abstract. Cobalt ions, in concentrations of 0 m M, block neuromuscular transmission in the frog sartorius muscle. The reduction in the e.p.p.

amplitude produced by Co 2+ is due to a decrease in the amount of transmitter released by a nerve impulse (mean quantum content). This reduction is associated with little change in the resting membrane potential of the muscle fibre or in the Cited by: William C.

Bowman BPharm, PhD, DSc, FIBiOl, FPS, FRSE, HonFFARCS, in Pharmacology of Neuromuscular Function (Second Edition), Introduction. On logical grounds the term ‘neuromuscular-blocking agent’ might be applied to any drug, the primary action of which is to interrupt neuromuscular transmission (e.g.

hemicholinium-3).In practice, however, the description is usually. Biophys J –, ), we have investigated several mechanisms of short-term facilitation at the frog neuromuscular junction. Our studies place constraints on previously proposed facilitation mechanisms and conclude that the presence of a second class of calcium sensor proteins distinct from synaptotagmin can explain known.

Desensitization, as represented by the progressive decline in the electromotive effects of depolarizing agents at the neuromuscular junction, was studied by observing the time course of changes in effective transmembrane resistance during the prolonged application of m M carbamylcholine to the postjunctional region of frog skeletal muscle by: A Ca 2+ -induced Ca 2+ Release Mechanism Involved in Asynchronous Exocytosis at Frog Motor Nerve Terminals J Gen Physiol (November, ) Changes in miniature endplate potential frequency during repetitive nerve stimulation in the presence of Ca2+, Ba2+, and Sr2+ at the frog neuromuscular by:.

Feltz A, Large WA, Trautmann A. Analysis of atropine action at the frog neutromuscular junction. J Physiol. Jul; (1)– Feltz A, Trautmann A. Desensitization at the frog neuromuscular junction: a biphasic process. J Physiol. Jan; – Ferry CB, Marshall AR.().

The fine structure of the neuromuscular junction of the frog. (). The influence of internal sodium on the behaviour of motor nerve endings. (). The measurement of synaptic delay and the time course of acetylcholine release at the neuromuscular junction.

(). The metabolism, storage and release of catecholamines. Recent : A. (Alistair) Mathie.References: Journal Articles: 1) Narahashi, T. Chemical as tools in the study of excitable membrane. Physiol. Rev.2) Narahashi, T., H.G. Haas and.