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B L Ginsborg

Publications and source records attributed to B L Ginsborg.

33 records · Page 2Linked to original sources
PubMed1972

The effect of adenosine on the release of the transmitter from the phrenic nerve of the rat.

1. The action of adenosine on neuromuscular transmission has been studied on the rat phrenic nerve-diaphragm preparation.2. Adenosine (0.025-10 mM) reversibly reduced the quantum content of end-plate potentials and the frequency of miniature end-plate potentials to about half the control values in preparations in which transmission was blocked with high Mg(2+) and/or low Ca(2+) concentrations. Where transmission was blocked with tubocurarine, the amplitude of end-plate potentials was reduced to about half the control values by adenosine.3. In solutions with very low Ca(2+) concentrations (no added Ca(2+) and 1 mM-EGTA) adenosine had a smaller effect on the frequency of miniature end-plate potentials.4. The effect of adenosine (0.025 and 0.05 mM) was abolished by theophylline (1.8 mM).5. The results are discussed in relation to the increase in cyclic AMP in brain slices caused by adenosine and the abolition of this effect by theophylline (Sattin & Rall, 1970).

Adenosine↗
PubMed1971

Prostaglandin E1 and noradrenaline at the neuromuscular junction.

The effects of prostaglandin E(1) (PGE(1)) on neuromuscular transmission in the frog nerve-sartorius muscle preparation were studied with intracellular recording techniques. PGE(1) was inactive in all concentrations examined; both spontaneous miniature end-plate potentials and evoked end-plate potentials were unchanged after preparations were bathed in up to 2.2x10(-5)M (8 mug/ml) PGE(1). PGE(1) did not prevent the increase in end-plate potential amplitude which frequently occurred on addition of noradrenaline to the bathing solution.

Animals↗
PubMed1971

On the presynaptic acetylcholine receptors in sympathetic ganglia of the frog.

1. Action potentials have been recorded extracellularly from individual preganglionic nerve terminals in the lumbar sympathetic chain of frogs (cf. Koketsu & Nishi, 1968).2. The action potentials were unaffected by changes in external Mg(2+) or Ca(2+) concentration, but were attenuated or even abolished by acetylcholine or carbachol. The effect on the presynaptic action potential was transient, in contrast to the blockade of synaptic transmission caused by these drugs, which as is well known persists indefinitely in their presence.3. In the presence of tubocurarine (5 x 10(-5)M), acetylcholine and carbachol had no effect on the presynaptic action potential.4. The action potentials were reduced by an increase in external K(+) concentration and abolished at between 9 and 16 mM K(+). Synaptic transmission persisted until the amplitude of the action potential was reduced to less than one third of its control value.5. It is concluded that although the presynaptic nerve is endowed with acetylcholine receptors, they are not the source of the long lasting blockade of synaptic transmission caused by cholinergic substances.

Acetylcholine↗
PubMedDate not supplied

Inhibition of acetylcholine release from preganglionic frog nerves by ATP but not adenosine.

ATP is known to be released in association with acetylcholine at synapses in the vertebrate peripheral nervous system. Exogenously applied ATP and its derivatives have been shown to reduce the release of acetylcholine, so it has been postulated that ATP has a role in the modulation of transmitter secretion. More recent results have suggested, however, that specific adenosine receptors are responsible for the inhibitory effects of adenosine derivatives on transmitter release, and ATP, if released, must be hydrolysed to adenosine to produce inhibition. The original hypothesis that ATP itself might inhibit acetylcholine secretion would be strengthened if it were found that adenosine is very much less potent than ATP as an inhibitor of ACh secretion. We report here results which show this is the case in sympathetic ganglia.

Acetylcholine↗