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Biomedical subjects

R Rahamimoff

Publications and source records attributed to R Rahamimoff.

At least 73 records · Page 4Linked to original sources
PubMed1973

Inhibitory action of Ruthenium red on neuromuscular transmission.

The effect of Ruthenium Red on synaptic transmission was examined at isolated junctions of the frog, by conventional methods for stimulation and intracellular recording. Ruthenium Red (2.5-10.0 muM) reduces the synaptic potential to subthreshold levels. An analysis of this phenomenon shows that the main action of Ruthenium Red is on the presynaptic nerve terminal where it decreases the number of quanta of transmitter liberated by the nerve impulse. It has the following additional effects: a reduction in the amplitude of the spontaneous miniature end plate potentials; an increase in their frequency; and an increase in delayed release of transmitter after a nerve impulse. Some of these results are discussed in terms of the known inhibitory action of Ruthenium Red on calcium transport across mitochondrial membranes.

Calcium↗
PubMed1973

Delayed release of transmitter at the frog neuromuscular junction.

1. After the end-plate potential (e.p.p.) there is an increase in the frequency of the miniature e.p.p.s. This delayed release of transmitter was studied at the frog neuromuscular junction, using conventional intracellular and extracellular recording techniques. E.p.p. amplitude was kept subthreshold by subnormal concentrations of activating divalent ions.2. The ratio delayed release: initial release had values between 2 and 140%, depending on the experimental conditions; it decreased with an increase in Ca concentration and quantal content.3. Delayed release is larger at low temperature than at room temperature.4. Delayed release is statistically independent of the amplitude of the preceding e.p.p.5. The time course of the decay of the delayed release is monotonic when strontium is the activating divalent ion; it shows a ;dip' in more than 50% of the cases when Ca activated release.6. The results were discussed in terms of the residual Ca ion hypothesis.

Animals↗
PubMed1972

Neuromuscular transmission: inhibition by manganese ions.

Manzganiese ions. are potent blocking argenits of synaptic transmission at the neuromuscular junction in the frog. The main site of action is the presynaptic nerve terminal, where the ions decr-ease the amount of transmitter liberated by a never impulse. The inihibition produced by manganese is reversible.

Action Potentials↗
PubMed1971

Activation of transmitter release by strontium and calcium ions at the neuromuscular junction.

1. The interaction between Ca and Sr ions on quantal transmitter release at the frog neuromuscular junction was studied, using conventional electrophysiological techniques.2. While Ca ions always activate transmitter release, the activating action of Sr ions depends on the Ca ion concentration in the medium; at low [Ca], strontium ions enhance the release, but at higher [Ca] they inhibit it. It is postulated that there is a [Ca] at which Sr ions do not affect transmitter liberation.3. When Sr activates release, its effect and the effect of Ca add in a more than linear fashion.4. Magnesium ions inhibit the release induced by Sr.5. The results can be explained by assuming that Ca and Sr act on the same site, at some stage of the process of quantal transmitter release. The affinity of both ions towards the sites is approximately the same, but the effectiveness of Sr is much smaller.

Action Potentials↗
PubMed1970

Neuromuscular synapse: stochastic properties of spontaneous release of transmitter.

The spontaneous quantal release of transmitter from the motor nerve endings is a random process which follows the Poisson theorem; the liberation of each quantum is independent of the release of previous quanta. Increase in the extracellular calcium concentration produces a statistical interdependence in the release of the spontaneously appearing packages.

Animals↗
PubMed1969

Strontium and quantal release of transmitter at the neuromuscular junction.

1. Previous work has shown that in calcium-free solutions nerve impulses invade the motor nerve terminals at the neuromuscular junction, but fail to release transmitter. In these conditions, strontium ions applied iontophoretically to a minute part of a junction, or to the whole muscle by bath application, restore to the nerve impulse its ability to release transmitter.2. As with calcium, the transmitter released in the presence of strontium is in the form of packages (quanta) whose release can be predicted from Poisson's Theorem.3. The mean number of quanta released by a nerve impulse increases with the concentration of strontium. Strontium is much less effective than calcium in equimolar concentrations.4. Transmitter quanta released in the presence of strontium evoke larger unit potentials than quanta released in the presence of calcium. The larger size of the Sr-unit potentials is caused by a prolongation of transmitter action, presumably due to a post-synaptic effect of strontium.5. Neuromuscular transmission was blocked in some fibres when the concentration of strontium was raised beyond 10 mM. This junctional block was presumably due to a failure in the propagation of nerve impulses.6. The post-stimulation increase in the frequency of miniature end-plate potentials, which is normally seen in calcium solutions, is also observed when calcium is substituted by strontium. The post-stimulation effect increases with the concentration of strontium.7. It is concluded that strontium can substitute for calcium in the process of quantal release of transmitter. The physico-chemical mechanism of this substitution remains unknown.

Animals↗
PubMed1968

A dual effect of calcium ions on neuromuscular facilitation.

1. The changes in neuromuscular facilitation produced by varying extracellular calcium and magnesium concentrations have been studied at the frog neuromuscular junction using intracellular recording and automatic averaging of responses.2. When [Ca] was elevated three effects were observed: a large increase in transmitter release by the first impulse; a decrease in facilitation at short intervals between impulses; and a prolongation of the time course of the facilitated release. If the release by the first impulse is kept at constant level, by raising both [Ca] and [Mg], facilitation becomes greater at all impulse intervals.3. The results have been discussed in terms of the hypothesis that the action of calcium is responsible for neuromuscular facilitation.

Animals↗
PubMed1968

Interaction between sodium and calcium ions in the process of transmitter release at the neuromuscular junction.

1. The interaction between Na and Ca ions on quantal transmitter release at the frog neuromuscular junction has been studied, using intracellular recording and averaging of responses.2. At low calcium concentrations, partial withdrawal of Na ions increases end-plate potential (e.p.p.) amplitudes and quantal content (m) and decreases the amplitude of the miniature e.p.p.s (m.e.p.p.s). Under these conditions the relation between [Ca] and m is highly non-linear. When plotted on double logarithmic co-ordinates withdrawal of [Na] causes a nearly parallel shift of this relation.3. Mutual interaction occurs between Ca, Na and Mg in transmitter release. With a constant low [Ca] in the medium, withdrawal of [Na] produces a smaller increase in m when [Mg] is high, than when [Mg] is low.4. In the presence of normal [Ca] (1.8 mM), [Na] withdrawal decreases the amplitude of the e.p.p. and produces a small decrease in m.5. The results can be explained by assuming that [Na] reduction has two mutually opposing effects on transmitter release: it makes more sites available for the action of Ca, and it lowers the amplitude of the action potential in the nerve terminals. The former effect dominates at low, the latter at high, calcium concentrations.

Journal Article↗
PubMed1967

Co-operative action a calcium ions in transmitter release at the neuromuscular junction.

1. The quantitative dependence of transmitter release on external calcium concentration has been studied at the frog neuromuscular junction, using intracellular recording and taking the amplitude of the end-plate potential (e.p.p.) as an index of the number of packets released.2. The relation between [Ca] and the e.p.p. is highly non-linear. The initial part of this relation on double logarithmic co-ordinates gives a straight line with a slope of nearly four (mean 3.78 +/- 0.2 S.D. in 28 experiments). Addition of a constant amount of Mg reduces the e.p.p. without altering the slope of the log e.p.p./log Ca relation.3. The slope of this logarithmic relation diminishes as [Ca] is raised towards the normal level.4. The results are explained quantitatively on the hypothesis that Ca ions combine with a specific site X on the nerve terminal forming CaX, and that the number of packets of acetylcholine released is proportional to the fourth power of [CaX].5. The analysis suggests that a co-operative action of about four calcium ions is necessary for the release of each quantal packet of transmitter by the nerve impulse.

Action Potentials↗