Extracellular chloride replacement by isethionate induces abnormal spontaneous release of transmitter at the frog neuromuscular junction

Ashford, M. L. J.; Wann, K. T.

doi:10.1111/j.1476-5381.1983.tb10513.x

Cited by 10 publications

(7 citation statements)

References 29 publications

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“…These g.m.e.p.ps also persisted in Ringer to which no Ca had been added. At control endplates, depolarization of motor nerve terminals by a raised external K concentration failed to induce g.m.e.p.ps (Ashford & Wann, 1983;Molenaar et al, 1987), even in the presence of a raised external Ca concentration as in the present study.…”

Section: Discussionsupporting

confidence: 71%

“…amplitude distributions were normal over 120min of recording (amplitude) c.v. of 25.7 + 0.9%, 15 endplates, 2 muscles). This is in marked contrast to the high reversible incidence of g.m.e.p.ps (>2 x modal) reported by Ashford & Wann (1983). The two studies used different procedures for mounting the preparations and it is possible that isethionate anions predispose the terminal for such a response.…”

Section: The Effect Of Mn Ions On the Phospholipase A2 Activity Ofcromentioning

confidence: 70%

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Early induction by crotoxin of biphasic frequency changes and giant miniature endplate potentials in frog muscle

Hawgood

Smith

Strong

1988

British J Pharmacology

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1 Following the addition of crotoxin (250nM) at the frog neuromuscular junction, there was an initial fall in frequency of miniature endplate potentials (m.e.p.ps), followed by a secondary rise which was characterized by the appearance of large spontaneous potentials (giants, g.m.e.p.ps) and an occasional large potential of the burst type.2 In the presence of 244-phenylpiperidino)cyclohexanol (AH5183, vesicamol), an inhibitor of vesicular acetylcholine uptake, the frequency of g.m.e.p.ps induced by crotoxin was reduced. 3 The characteristic changes in m.e.p.p. frequency and amplitude distribution were absent with crotoxin in Sr-EGTA Ringer. In the presence of high concentrations of Mn (3.6 or 5.4mm with 0.9mm Ca), the crotoxin-induced initial fall and the onset of the secondary rise in m.e.p.p. and g.m.e.p.p. frequencies were slower. The timing of these phases was unaffected by Ca concentrations ranging from 6.3 to 0.9 mm. 4 High concentrations of Mn ions partially inhibited the phospholipase A2 activity of crotoxin on artificial phospholipid membranes. This also supports the involvement of the Ca-dependent phospholipase A2 subunit in both phases of the physiological action of the toxin. 5 G.m.e.p.ps were associated with a moderate increase in m.e.p.p. frequency (2-3 s1) and were of a time-course similar to that of m.e.p.ps. They persisted after washing with medium lacking Ca ions and in the presence of Ca-Mn Ringer that blocked evoked responses. 6 It is concluded that crotoxin, acting through its phospholipase A2 subunit, produces specific disturbances of synaptic exocytosis and vesicle formation in the axolemma of the motor nerve terminal which lead to biphasic changes in m.e.p.p. frequency and the onset of large spontaneous potentials.

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Section: Discussionsupporting

confidence: 71%

Section: The Effect Of Mn Ions On the Phospholipase A2 Activity Ofcromentioning

confidence: 70%

Early induction by crotoxin of biphasic frequency changes and giant miniature endplate potentials in frog muscle

Hawgood

Smith

Strong

1988

British J Pharmacology

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“…frequency, in contrast to the m.e.p.p. frequency, is not influenced when the K+ concentration of the incubation medium is raised only P. C. MOLENAAR, B. S. OEN AND R. L. POLAK moderately (Pecot-Dechavassine, 1976;Molgo & Thesleff, 1982;Ashford & Wann, 1983;present experiments). Moreover, the m.e.p.p.…”

Section: Discussionmentioning

confidence: 86%

Effect of chloride ions on giant miniature end‐plate potentials at the frog neuromuscular junction.

Molenaar

Oen

Polak

1987

The Journal of Physiology

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SUMMARY1. Frog sartorius muscles were incubated in Ringer solutions with a raised K+ concentration (high K+) and then allowed to recover in medium with a normal K+ concentration. During the recovery period miniature end-plate potentials (m.e.p.p.s) were recorded with intracellular electrodes. In addition, the acetylcholine (ACh) released from muscles in the presence of high K+ was measured by a mass spectrometric method.2. Incubation in a high-K+ medium induced the appearance of giant miniature end-plate potentials (g.m.e

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“…Similar potentials are observed at the frog neuromuscular junction (Fatt and Katz, 1952;). Isoethionate replacement of chloride, on the other hand, stimulates their frequency (Ashford and Wann, 1983). Isoethionate replacement of chloride, on the other hand, stimulates their frequency (Ashford and Wann, 1983).…”

Section: Physiological and Pharmacological Importancementioning

confidence: 99%

“…In the frog they are enhanced in frequency after intense nerve stimulation (Molgo, 1982; Molenaar et al, 1987) and are blocked if chloride is replaced by propionate in the extracellular solution (Molenaar et al, 1987). Isoethionate replacement of chloride, on the other hand, stimulates their frequency (Ashford and Wann, 1983). Slow, spontaneous calcium-insensitive mepp have also been observed at inhibitory and excitatory motor junctions of the crayfish (Finger and Martin, 1984;1986) and at the excitatory junction of the locust (Cull-Candy and Miledi, 1982).…”

Section: Physiological and Pharmacological Importancementioning

confidence: 99%

Spontaneous Transmitter Release at the Neuromuscular Junction

Thesleff

1988

Fundamemntal Clinical Pharma

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The classical studies of Katz and co-workers have shown that nerve impulses release quanta of acetylcholine at the neuromuscular junction. This release is regulated by presynaptic calcium and accounts for the trans-synaptic transmission of nerve impulses. In resting conditions it gives rise to small spontaneous potentials, i.e. miniature endplate potentials. In addition these investigators described a spontaneous molecular leakage of acetylcholine from the motor nerve. I have studied a third type of acetylcholine release. It is a spontaneous intermittent secretion of acetylcholine which postsynaptically causes large, generally slow rising potentials. This release is unaffected by presynaptic calcium and is therefore not influenced by nerve activity. The acetylcholine responsible for these potentials comes from the same pool of transmitter as that liberated by nerve impulses. The observation that the release is blocked by drugs that prevent the accumulation of acetylcholine into synaptic vesicles indicates that the secretion originates from clusters of vesicles or large vesicle-like structures in the nerve terminal. This type of release is present at a low frequency at normal neuromuscular junctions. It is markedly accelerated whenever the calcium-dependent quantal release of acetylcholine is blocked or impaired. The drug 4-aminoquinoline selectively stimulates this release. I speculate that this type of transmitter secretion is important for the development of synaptic connexions.

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Extracellular chloride replacement by isethionate induces abnormal spontaneous release of transmitter at the frog neuromuscular junction

Cited by 10 publications

References 29 publications

Early induction by crotoxin of biphasic frequency changes and giant miniature endplate potentials in frog muscle

Early induction by crotoxin of biphasic frequency changes and giant miniature endplate potentials in frog muscle

Effect of chloride ions on giant miniature end‐plate potentials at the frog neuromuscular junction.

Spontaneous Transmitter Release at the Neuromuscular Junction

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