The action of facilitatory drugs on the isolated tenuissimus muscle of the cat

Blaber, L. C.; Christ, Daryl

doi:10.1016/0028-3908(67)90047-0

Cited by 32 publications

(19 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…was increased whilst the amplitude of the miniature endplate potential (m.e.p.p.) was unaffected (Blaber & Christ, 1967). In the latter study it was concluded that edrophonium increased transmitter release in curarized cat skeletal muscle, since there was no change in the time course of the e.p.p.…”

Section: Introductionmentioning

confidence: 83%

See 1 more Smart Citation

The mechanism of the facilitatory action of edrophonium in cat skeletal muscle

Blaber

1972

British J Pharmacology

View full text Add to dashboard Cite

Summary The effects of edrophonium have been observed in the transversely cut tenuissimus muscle of the cat. Concentrations of edrophonium 10−7M to 10−5M increased the amplitude of the end‐plate potential (e.p.p.) but produced no greater increase in time course than previously observed in curarized muscle. When the e.p.p. and gross nerve action potential were recorded simultaneously, antidromic discharges were observed in the motor nerve concomitantly with repetitive e.p.ps in the presence of edrophonium. Edrophonium produced no effect on the input resistance or equilibrium potential of the end‐plate. The fractional release of transmitter was significantly increased by edrophonium but there was no increase in the quantal release of transmitter in the transversely cut muscle preparation. In curarized muscle edrophonium also increased the quantal release, the size of the available store of transmitter and the rate of refilling of the available store. It is concluded that edrophonium facilitates transmission to skeletal muscle by inducing a repetitive antidromic discharge in the nerve, following orthodromic stimulation. The antidromic discharge propagates by axon reflex to other nerve terminals of the same motor unit producing repetitive e.p.ps. It is also suggested that edrophonium antagonizes tubocurarine by acting as a partial agonist at the motor nerve terminal.

show abstract

Section: Introductionmentioning

confidence: 83%

“…It was suggested (Blaber & Christ, 1967) that this mechanism could still apply to edrophonium, since Eccles et al (1942) had previously shown that tubocurarine would decrease the duration of the e.p.p. prolonged by the action of an anticholinesterase drug.…”

Section: Introductionmentioning

confidence: 99%

The mechanism of the facilitatory action of edrophonium in cat skeletal muscle

Blaber

1972

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…This was due to the increased fractional release being offset by a reduced rate of filling of the available store and a reduction in the size of the available store to 59% of the control value. The quantum size was reduced to approximately 2%, assuming the control quantum size to be equal to the amplitude of the miniature end-plate potentials (0*6 mV) (Blaber & Christ, 1967).…”

Section: Tubocurarinementioning

confidence: 99%

“…The preparation and technique used have been described previously (Blaber & Christ, 1967;Blaber, 1970 (Blaber, 1972)) formed the data for a computer programme (CDC 6,600).…”

Section: Methodsmentioning

confidence: 99%

The prejunctional actions of some non‐depolarizing blocking drugs

Blaber

1973

British J Pharmacology

View full text Add to dashboard Cite

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.

show abstract

“…The theory has been criticized (Hubbard, 1970), but supporting evidence has accumulated in the intervening years (see Miyamoto, 1978). At the mammalian neuromuscular junction cholinergic agonists and anticholinesterases stimulate spontaneous release (Boyd & Martin, 1956;Blaber & Christ, 1967;Laskowski & Dettbarn, 1975) the action of carbachol being reversible and antagonized by curare (Miyamoto & Volle, 1974). There is considerable evidence that cholinoceptive sites are present on these presynaptic terminals and cholinesterase inhibitors are able to initiate antidromic impulses in the mammalian motor nerve, this effect again being abolished by treatment with curare (Masland & Wigton, 1940; Riker, Werner, Roberts & Kuperman, 1959;Blaber, 1972).…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effects of cholinergic agents on the release of transmitter at the frog neuromuscular junction.

Duncan¹,

Publicover²

1979

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. The cholinesterase inhibitors neostigmine, edrophonium and eserine (7 x 10-7 M) reduced m.e.p.p. frequency by some 50 % at the frog neuromuscular junction.Neostigmine also produced a small reduction in quantal content.2. Tetraisopropylpyrophosphoramide, with a high specificity for non-specific cholinesterase, has a similar effect on m.e.p.p. frequency but ambenonium, with a high specificity for acetylcholinesterase, was markedly less effective in this respect.3. Carbachol (10-5 M) and the muscarinic agonists muscarine and metacholine (7 x 10-7 M) also reduced the rate of spontaneous release.4. 6. It is concluded that non-specific cholinesterases present on the presynaptic terminals can act as inhibitory muscarinic cholinergic receptors. This form of presynaptic inhibition at the amphibian neuromuscular junction contrasts with that described in the mammalian preparation in which the sites are blocked by Dtubocurarine and are excitatory.

show abstract

The action of facilitatory drugs on the isolated tenuissimus muscle of the cat

Cited by 32 publications

References 24 publications

The mechanism of the facilitatory action of edrophonium in cat skeletal muscle

The mechanism of the facilitatory action of edrophonium in cat skeletal muscle

The prejunctional actions of some non‐depolarizing blocking drugs

Inhibitory effects of cholinergic agents on the release of transmitter at the frog neuromuscular junction.

Contact Info

Product

Resources

About