The Effects of Tetraphenylboron on Neuromuscular Transmission in the Frog

Marshall, Ian; Parsons, Rodney L.

doi:10.1111/j.1476-5381.1975.tb07572.x

Cited by 13 publications

(5 citation statements)

References 16 publications

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“…In the case of TPB this drop in frequency was accompanied by a reduction in m.e.p.p. amplitude which was not due to a post-junctional blocking action (Marshall & Parsons, 1975 . Thus the fall in m.e.p.p.…”

Section: Discussionmentioning

confidence: 83%

“…The high m.e.p.p. frequency that appears after washing of TPB-treated tissues, and the evidence from studies on evoked transmitter release that the probability of release remains enhanced even after prolonged perfusion of TPB (Marshall & Parsons, 1975), suggests that small quantities of acetylcholine, producing effects indistinguishable from the noise, probably continue to be released, despite the apparent abolition of m.e.p.p. activity.…”

Section: Discussionmentioning

confidence: 99%

“…Amongst the most striking effects of tetraphenylboron described in the previous paper (Marshall & Parsons, 1975) were a marked increase in spontaneous transmitter release, and a subsequent time-dependent decrease in miniature endplate potential (m.e.p.p.) amplitude and frequency.…”

Section: Introductionmentioning

confidence: 85%

“…Convenitional intracellular recording techniques, as described in the previous paper (Marshall & Parsons, 1975), were used to record miniature endplate potentials (m.e.p.ps) fromo the frog sartorius muscle. ['FB, dissolved in K+-deficient Ringer solution (Marshall & Parsons, 1975), was applied to individlual neuromuscular junctions by l'resent address: Department ot Physiology and Plharmlacology, University ot Strathtcl de, Glasgow (G I I XW. local microperfusion.…”

Section: Metlhodsmentioning

confidence: 99%

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The Effects of Tetraphenylboron on Spontaneous Transmitter Release at the Frog Neuromuscular Junction

Marshall¹,

Parsons²

1975

British J Pharmacology

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1The effects of tetraphenylboron (TPB) on spontaneous transmitter release were studied in the frog sartonius muscle preparation. 2 TPB (0.001-1 mM) produced a time-dependent increase in miniature endplate potential (m.e.p.p.) activity that was not sustained. TPB (0.1 mM) produced similar effects on m.e.p.p. frequency in normal Ringer solutions, in the absence of Ca2+ or CF-and in the presence of excess Ca2+ and of tetrodotoxin. The effect of TPB (0.01 mM) was reduced but not abolished in the absence of Ca2+. probably by a combination of rapid release and concomitant inhibition of transmitter storage.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 85%

Section: Metlhodsmentioning

confidence: 99%

See 2 more Smart Citations

The Effects of Tetraphenylboron on Spontaneous Transmitter Release at the Frog Neuromuscular Junction

Marshall¹,

Parsons²

1975

British J Pharmacology

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“…It decreases the amplitude of the spontaneous MEPPs, and the magnitude of the reduction increases with time (23). In concentrations of 50 ,uM or higher, it has no effect on the depolarization produced by carbachol applied by microperfusion (24). It was suggested that tetraphenylborate may reduce the concentration of AcCho in the vesicles (23).…”

Section: Discussionmentioning

confidence: 99%

Is an acetylcholine transport system responsible for nonquantal release of acetylcholine at the rodent myoneural junction?

Edwards¹,

Doležal²,

Tuček³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

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Experiments were performed to investigate the effects on the spontaneous, nonquantal release of acetylcholine (AcCho) from motor nerve terminals of substances known to inhibit the AcCho transport system present in cholinergic synaptic vesicles. In mouse diaphragms, the hyperpolarization normally produced by d-tubocurarine in the end. plate area of muscle fibers that had been treated by an anticholinesterase was partly or completely blocked by 2-(4-phenylpiperidino)cyclohexanol (AH5183, 0.1-1 ,sM), quinacrine (0.1 1AM), and tetraphenylborate (1 IAM). Since the sensitivity of the subsynaptic area to AcCho was not changed, the block of the hyperpolarizing action of d-tubocurarine indicated an inhibition of the spontaneous, nonquantal release of AcCho. This was confirmed in experiments on rat diaphragm using direct radioenzymatic measurement of the AcCho released into the incubation medium. The release of AcCho from the innervated diaphragm was decreased by about 50% in the presence of AH5183 (0.01-1 FAM) and by 42% in the presence of quinacrine (0.1-1 FM). The AcCbo released was presumably neural, since the release of AcCho from 4-day denervated diaphragms was not diminished by either AH5183 or quinacrine. The results indicate that the spontaneous release of AcCho from the motor nerve terminals is highly sensitive to low concentrations of specific inhibitors and is probably mediated by a carrier. It is proposed that spontaneous release is due to the incorporation into the membrane of the nerve terminal during exocytosis of the vesicular transport system responsible for moving AcCho into the vesicle.Acetylcholine (AcCho) is released from the nerve terminal of the neuromuscular junction in several ways. There is electrophysiological evidence for the random release of quanta of AcCho, which gives rise to small, transient postsynaptic depolarizations (miniature endplate potentials or MEPPs), and for the stimulation evoked multiquantal release, which gives rise to endplate potentials (1).In The mechanism underlying the nonquantal release of AcCho is unknown. Synaptic vesicles isolated from the electric organ of Torpedo have been shown to take up AcCho by an active process (9). If the transport system responsible for this is present in vesicles in the nerve terminal of the neuromuscular junction, and if it retains its orientation following the incorporation of the vesicle membrane into the axon membrane during exocytosis, then it would move AcCho from the axoplasm into the extracellular space. We have investigated the effects on nonquantal release of several agents that block the transport of AcCho by vesicles (10, 11) to determine whether the release may be due to this transport system. Nonquantal release has been measured electrophysiologically and by direct analysis of bath AcCho. METHODSElectrophysiological Experiments. The experiments were performed on hemidiaphragms dissected from decapitated female white specific-pathogen-free mice. The thoracic side of the diaphragm was carefully cleaned of pleura, which ...

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Bor und spezielle Borverbindungen

Kliegel¹

1980

BOR in Biologie, Medizin Und Pharmazie

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The Effects of Tetraphenylboron on Neuromuscular Transmission in the Frog

Cited by 13 publications

References 16 publications

The Effects of Tetraphenylboron on Spontaneous Transmitter Release at the Frog Neuromuscular Junction

The Effects of Tetraphenylboron on Spontaneous Transmitter Release at the Frog Neuromuscular Junction

Is an acetylcholine transport system responsible for nonquantal release of acetylcholine at the rodent myoneural junction?

Bor und spezielle Borverbindungen

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