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Biomedical subjects

S F Jones

Publications and source records attributed to S F Jones.

28 records · Page 2Linked to original sources
PubMed1971

The effect of temperature change upon transmitter release, facilitation and post-tetanic potentiation.

1. End-plate potentials (e.p.p.s) and miniature end-plate potentials (m.e.p.p.s) were intracellularly recorded from rat diaphragm phrenic nerve preparations in vitro at temperatures between 7 degrees and 40 degrees C.2. The quantal content of e.p.p.s and the frequency of m.e.p.p.s showed broadly similar relationships with temperature, with maxima about 20 degrees and above 39 degrees C.3. Analysis of the change in e.p.p. quantal content showed that the maximum about 20 degrees C was accompanied by a similar maximum of p, the probability of release of quanta. The maximum above 39 degrees C was associated with a rise in n, a presynaptic store of material needed for release.4. The rate at which transmitter could be mobilized was linear in an Arrhenius plot with an apparent activation energy of 25 kcal deg(-1).5. Facilitation and post-tetanic potentiation (PTP) were shown to be entirely attributable to changes in p.6. It is suggested that facilitation and PTP have a common basis and that the (temperature-dependent) rate of Ca removal from intracellular sites at which it exerts its action is as important a determinant of the magnitude of quantal release as is the amount of Ca combining with these sites.

Activation Analysis↗
PubMed1971

An investigation of experimental myasthenia gravis.

Guinea-pigs were immunized with antigen prepared from calf thymus and muscle, and from guinea-pig thymus, and rats were immunized with antigen prepared from rat thymus and rat muscle. There was an increased incidence of delayed hypersensitivity and circulating thymus antibodies in the immunized guinea-pigs and an increased incidence of thymitis in the immunized guinea-pigs and rats. However, when compared with control animals, there was no electrophysiological evidence of impairment of neuromuscular transmission in the immunized animals.

Action Potentials↗
PubMed1970

The effects of nerve stimulation and hemicholinium on synaptic vesicles at the mammalian euromuscular junction.

1. Electron micrographs of nerve terminals in rat phrenic nerve-diaphragm preparations have been studied. This has been done before and after prolonged nerve stimulation. The effectiveness of nerve stimulation has been monitored by intracellular micro-electrode recordings from the muscle cells.2. Characteristic changes in the form and distribution of the nerve terminal mitochondria were noted after nerve stimulation.3. Synaptic vesicle numbers in the region of nerve terminal less than 1800 A from the synaptic cleft were significantly greater in tissue taken 2 and 3 min after nerve stimulation, than in unstimulated preparations.4. The long and short diameters of the synaptic vesicle profiles less than 1800 A from the synaptic cleft were measured. Analysis of the distribution of the diameters indicated synaptic vesicles to be basically spherical structures. Estimates of synaptic vesicle volume were made from the measurements. Synaptic vesicle volume was significantly reduced in tissue taken 2 and 4 min following nerve stimulation.5. If hemicholinium, a compound which inhibits acetylcholine synthesis, was present during the period of nerve stimulation, much greater reductions in synaptic vesicle volume occurred. Synaptic vesicle numbers in the region of nerve terminal less than 1800 A from the synaptic cleft were also reduced, compared with unstimulated control preparations.6. These results are regarded as support for the hypothesis that the synaptic vesicles in nerve terminals at the mammalian neuromuscular junction represent stores of the transmitter substance, acetylcholine.

Acetylcholine↗
PubMed1970

Some effects of nerve stimulation andhemicholinium on quantal transmitter release at the mammalian neuromuscular junction.

1. Rat phrenic nerve-diaphragm preparations have been used to assess some effects of prolonged nerve stimulation on transmitter release.2. The amplitude of the end-plate potentials evoked by prolonged repetitive nerve stimulation fell gradually during stimulation. Most of this fall was due to a reduction in the number of transmitter quanta released by each nerve impulse; however there was also a small reduction in the muscle cell depolarization produced by each quantum of transmitter.3. Repetitive nerve stimulation also produced a small reduction in the amplitude of the miniature end-plate potentials. Recovery of amplitude occurred within about 7-8 min of ceasing stimulation.4. A much greater reduction in miniature end-plate potential amplitude accompanied prolonged nerve stimulation if hemicholinium was present in the bathing solution.5. Estimates of the ;readily available transmitter' (Elmqvist & Quastel, 1965b) were made at intervals following prolonged nerve stimulation. Readily available transmitter was reduced, and recovered over approximately 15 min.6. The relationship of these changes to the changes in nerve terminal synaptic vesicle numbers and volumes induced by similar prolonged nerve stimulation (Jones & Kwanbunbumpen, 1970) is discussed.

Animals↗
PubMed1968

On the mechanism by which calcium and magnesium affect the spontaneous release of transmitter from mammalian motor nerve terminals.

1. The frequency of miniature end-plate potentials (m.e.p.p.s) was recorded from neuromuscular junctions in rat diaphragm phrenic nerve preparations in vitro after preparations had soaked in solutions containing Ca in concentrations between 10(-10) and 10(-2)M and a similar range of [Mg].2. Ethylenediamine tetra-acetate (EDTA) and ethyleneglycol bis (beta-aminoethyl ether) tetra-acetate (EGTA) buffers were added to prepare solutions with [Ca] and [Mg] below 10(-4)M. A computer program was used to estimate the free [Ca(2+)] in these solutions, and it was shown that the effects of Ca could be attributed to the free [Ca(2+)] in the bathing solution.3. M.e.p.p.s could still be detected without difficulty after soaking preparations for 6-8 hr in solutions containing EDTA or EGTA buffers and no added Ca. The basal frequency was unchanged upon exhibition of Ca in concentrations up to 10(-5)M and/or Mg in concentrations up to 10(-3)M.4. Ca in concentrations of and above 10(-4)M accelerated m.e.p.p. frequency from the basal level. This effect reached a maximum in [Ca] of 10 mM and raising the [Ca] above this level did not further change frequency. These effects were explained by the combination of Ca molecules with a nerve terminal receptor site. It was postulated that this combination allosterically activated the spontaneous release mechanism.5. Mg could accelerate m.e.p.p. frequency in the absence of added Ca. The interactions of Ca and Mg upon m.e.p.p. frequency indicated that Ca and Mg competed for the same sites.6. Raising the [H(+)] of the bathing medium accelerated m.e.p.p. frequency. This effect was thought to be exerted partly by combination with the same receptor sites as Ca and Mg and partly by variation of the ionization of the CaCl(2) of the bathing solution.

Acetates↗
PubMed1968

On the mechanism by which calcium and magnesium affect the release of transmitter by nerve impulses.

1. The relationship between the quantal content of end-plate potentials (e.p.p.s) and the bathing [Ca] and [Mg] was determined at neuromuscular junctions in the rat diaphragm in vitro.2. E.p.p.s were recorded intracellularly from preparations exposed to solutions with [Ca] between 0.05 and 10 mM and [Mg] between 0.1 and 12.5 mM. The quantal content of e.p.p.s was increased by raising the [Ca] over this range and decreased by raising the [Mg]. There appeared to be competition of Mg with Ca at three sites in the nerve terminal membrane.3. A kinetic scheme based on competition of Ca and Mg at three sites could quantitatively explain the effects of Ca and Mg upon the quantal content of e.p.p.s and also the effects of these ions upon miniature end-plate potential frequency.

Acetylcholine↗
PubMed1968

An examination of the effects of osmotic pressure changes upon transmitter release from mammalian motor nerve terminals.

1. When the frequency of miniature end-plate potentials (m.e.p.p.s) was measured at neuromuscular junctions in rat diaphragm nerve preparations in vitro bathed in solutions having osmolarities between 200 and 700 m-osmoles/l. it was found that m.e.p.p. frequency was transiently increased by exposure to osmotic gradients exceeding 75 m-osmoles/l., and then declined, within 1 hr, to a steady level slightly higher than the control level of frequency. Smaller osmotic gradients caused a maintained increase in m.e.p.p. frequency. E.p.p. quantal content was initially increased and later profoundly decreased upon exposure of preparations to solutions with an osmotic pressure of 500 or 600 m-osmoles/l. but was unaffected by less hypertonic solutions.2. Variation of the Ca or Mg content of the bathing solutions did not alter these effects of osmotic pressure on the early transient increase in m.e.p.p. frequency or e.p.p. quantal content but affected the late steady increase in m.e.p.p. frequency.3. The value of the transient increase in m.e.p.p. frequency was exponentially related to the osmotic gradient in the range 0-300 m-osmoles/l. with a Q(10) of 1.95 (range 11-34 degrees C). Greater osmotic gradients did not further increase m.e.p.p. frequency. Variation of the ionic strength of the bathing medium did not influence osmotic effects upon frequency.4. The discrepancy between the effects of osmotic gradients upon spontaneous and nerve-impulse induced transmitter release was explained by an occlusion of the osmotic effects by depolarization of nerve terminals. Time-course studies showed that in the presence of 20 mM-KCl the m.e.p.p. frequency increase in response to an increase in osmotic pressure was small and was followed by a reduction in frequency to below control levels while osmotic pressure changes had no immediate effect upon m.e.p.p. frequency in solutions containing 30 mM-KCl.5. It was concluded that increased osmotic gradients could release transmitter by a mechanism independent of Ca and of nerve terminal depolarization.6. It is suggested that the initial transient effects of changes of osmotic gradient upon transmitter release are related to flow of water through the nerve terminal membrane, while the later effects are related to nerve terminal volume changes.

Animals↗