Characteristics of crayfish neuromuscular facilitation and their calcium dependence

Zucker, Robert S.

doi:10.1113/jphysiol.1974.sp010642

Cited by 103 publications

(64 citation statements)

References 37 publications

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“…However, e.j.p.s could still be recorded in deep fibres, and very slight movement occurred at very high frequencies (over 30 Hz). Apparently, y-MG fails to penetrate below the muscle surface fibres (see Zucker, 1974a).…”

Section: Resultsmentioning

confidence: 99%

Crayfish neuromuscular facilitation activated by constant presynaptic action potentials and depolarizing pulses

Zucker¹

1974

The Journal of Physiology

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SUMMARY1. Experiments were conducted to test the hypothesis that facilitation of transmitter release in response to repetitive stimulation of the exciter motor axon to the crayfish claw opener muscle is due to an increase in the amplitude or duration of the action potential in presynaptic terminals. No consistent changes were found in the nerve terminal potential (n.t.p.) recorded extracellularly at synaptic sites on the surface of muscle fibres.2. Apparent changes in n.t.p. are attributed to three causes. (i) Some recordings are shown to be contaminated by non-specific muscle responses which grow during facilitation.(ii) Some averaged n.t.p.s exhibit opposite changes in amplitude and duration which suggest a change in the synchrony of presynaptic nerve impulses at different frequencies.(iii) Some changes in n.t.p. are blocked by y-methyl glutamate, an antagonist of the post-synaptic receptor, which suggests that these changes are caused by small muscle movements.3. The only change in n.t.p. believed to represent an actual change in the intracellular signal is a reduction in n.t.p. amplitude to the second of two stimuli separated by a brief interval.4. Tetra-ethyl ammonium ions increase synaptic transknission about 20 % and prolong the n.t.p. about 15 %. This result suggests that an increase in n.t.p. large enough to increase transmission by the several hundred per cent occurring during facilitation would be detected.5. The nerve terminals are electrically excitable, and most synaptic sites have a diphasic or triphasic n.t.p., which suggests that the motor neurone terminals are actively invaded by nerve impulses.6. When nerve impulses are blocked in tetrodotoxin, depolarization of * Present address:

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Section: Resultsmentioning

confidence: 99%

Crayfish neuromuscular facilitation activated by constant presynaptic action potentials and depolarizing pulses

Zucker¹

1974

The Journal of Physiology

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“…Reduced [Ca2+]e, at a level of 0.1mM free-Ca2+ (buffered in Mg2 +-EDTA; Zucker, 1974) was tested in five preparations; in four of these, more impulses were required to produce blockage and in one there was no significant difference. Elevated [Ca2 +]e appeared to have the opposite effect.…”

Section: Effects Of Changing the Bath Composition And Temperaturementioning

confidence: 99%

Mechanisms of action potential propagation failure at sites of axon branching in the crayfish.

Smith¹

1980

The Journal of Physiology

134

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SUMMARY1. The phenomena leading to action potential conduction block during repetitive stimulation of the excitor axon of the opener muscle in the crayfish walking leg were studied.2. Action potentials, recorded extracellularly with micro-electrodes, failed to propagate past sites of axonal bifurcation following at least 3000 impulses; reduction of the rate or brief cessation of stimulation resulted in restored conduction.3. Failure occurred initially at branch points located most peripherally and then more centrally as stimulation continued; this centripetal progression of the site of block resulted in a stepwise reduction of the number of synaptic terminals from which transmitter was released.4. Prior to conduction failure, the conduction velocity and the sodium inward current of the action potentials decreased.5. Local application of hyperpolarizing current or of physiological saline with low [K+] in the vicinity of a block can restore propagation; thus depolarization of the membrane most probably causes failure.6. Soaking the preparation for as long as 2 hr in the metabolic inhibitor 2,4-dinitrophenol had no effect on the number of stimulus impulses before initial conduction block; however, the time required for recovery from the failure was prolonged.7. The number of impulses prior to block was related directly to the temperature of the preparation; this had a Q10 calculated to be about 1*3.8. It is suggested that during repetitive activity, the K + gradient across the membrane is reduced, resulting in depolarization and eventually in conduction failure.

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“…In the classic "residual calcium model" (Katz and Miledi, 1968) a highly nonlinear relationship between [Ca2+] and release is used to account for the observation that increased residual calcium produces a large enhancement of action potential-evoked release without causing a continuously high rate of spontaneous release. This model, while qualitatively able to account for the rapid decay of short-term facilitation, is unable to account quantitatively for many properties of the buildup and decay of synaptic enhancement (e.g., Zucker, 1974b;Zucker and Fogelson, 1986;Magleby, 1987). More recent modifications of the residual Ca*+ model for the shortestlasting phases of facilitation (persisting for = 1 set or less) have suggested that the decay of this process is set by the reverse rate of a Ca2+-activated process such as the dissociation rate of Ca2+ from a facilitating site, rather than the decay of free Ca*+ in the cytoplasm (Balnave and Gage, 1974;Stanley, 1986;Robitaille and Charlton, 199 1;Yamada and Zucker, 1992).…”

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A quantitative measurement of the dependence of short-term synaptic enhancement on presynaptic residual calcium

1994

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We simultaneously measured presynaptic free calcium ion concentration ([Ca2+]i) and synaptic strength at the crayfish claw opener neuromuscular junction (nmj) under a variety of experimental conditions. Our experiments were designed both to test the hypothesis that elevated [Ca2+]i is necessary and sufficient for the induction of a form of synaptic enhancement that persists for several seconds after tetanic stimulation--augmentation--and to determine the quantitative relationship between elevated [Ca2+]i and this enhancement. Action potential trains increased [Ca2+]i and enhanced transmission. During the decay phase of synaptic enhancement known as augmentation (time constant of decay approximately 7 sec at 20 degrees C with < 200 microM fura-2 in terminals), [Ca2+]i was elevated 700 nM or less above rest and an essentially linear relationship between [Ca2+]i and enhancement was observed. Introduction of exogenous Ca2+ buffers into the presynaptic terminal slowed the buildup and recovery kinetics of both [Ca2+]i and the component of synaptic enhancement corresponding to augmentation. The slope of the relationship relating delta [Ca2+]i to augmentation was not changed. The time course of augmentation and recovery of [Ca2+]i remained correlated as the temperature of the preparation was changed from about 10 degrees C to 20 degrees C, but the quantitative relationship of enhancement to [Ca2+]i was increased more than two- to threefold. During moderate frequency trains of action potentials, a slowly developing component of the total synaptic enhancement was approximately linearly related to residual [Ca2+]i measured with fura-2. The quantitative relationship between [Ca2+]i and this component of synaptic enhancement during trains was the same as that during synaptic augmentation after trains.(ABSTRACT TRUNCATED AT 250 WORDS)

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Characteristics of crayfish neuromuscular facilitation and their calcium dependence

Cited by 103 publications

References 37 publications

Crayfish neuromuscular facilitation activated by constant presynaptic action potentials and depolarizing pulses

Crayfish neuromuscular facilitation activated by constant presynaptic action potentials and depolarizing pulses

Mechanisms of action potential propagation failure at sites of axon branching in the crayfish.

A quantitative measurement of the dependence of short-term synaptic enhancement on presynaptic residual calcium

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