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Biomedical subjects

R L Volle

Publications and source records attributed to R L Volle.

At least 55 records · Page 3Linked to original sources
PubMed1975

Pre- and postjunctional neuromuscular blockade by carbachol.

Carbachol, when applied to the bathing Ringer solution of frog sartorius muscles, caused depolarization of the endplate and a blockade of endplate potentials (EPP's), miniature EPP's (mepp's) and the iontophoretic acetylcholine potential. In muscles treated with an analog of hemicholinium-3, alpha, alpha'bis(dimethylammonium acetaldehyde diethylacetal)-p-p'-diacetylbiphenyl dibromide (DMAE), depolarization of the endplate by carbachol was blocked and the blockade by carbachol of the iontophoretic acetylcholine potential was prevented. These responses to carbachol were attributed to a postjunctional action that was antagonized by DMAE. In contrast, the blockade by carbachol of EPP's and mepp's was enhanced in DMAE-treated muscles at a time when carbachol-induced depolarization was blocked. This response to carbachol was attributed to a pre-junctional action. Carbachol either blocked transmitter release by a mechanism that was insensitive to DMAE or enhanced the prejunctional blocking actions of DMAE. Succinylcholine had actions similar to carbachol. DMAE prevented depolarization by succinylcholine but enhanced neuromuscular blockade by succinylcholine. SKF 525-A (beta-diethylaminoethyl diphenylpropylacetate hydrochloride), like DMAE, prevented depolarization but not transmission blockade caused by carbachol.

Acetylcholine↗
PubMed1975

Modification by lithium of transmitter release at the neuromuscular junction of the frog.

Complete or partial replacement of Na+ by Li+ resulted in a progressively developing increase in the amplitude and quantal content of end-plate potentials of the frog neuromuscular junction. Analysis of frequency facilitation curves and estimations of the binomial parameters of release indicate that Li+ caused an increase in the probability of transmitter release. Li+ also caused a time dependent increase in the frequency of miniature end-plate potentials. The responsiveness of the miniature end-plate potentials to Li+ was depressed by elevated Ca++ and enhanced by elevated K+. Collectively, the effects of Li+ on transmitter release can be attributed to the accumulation by the nerve terminals of Li+ resulting on an increased level of intracellular Ca++.

Animals↗
PubMed1974

Enhancement by carbachol of transmitter release from motor nerve terminals.

In the endplates of rat phrenic nerve-diaphragm, application of the acetylcholine-like compound, carbachol, causes a marked increase in transmitter release, as measured electrophysiologically using miniature endplate potential frequency. Washing out of carbachol reverses the increase in frequency. The ability of carbachol to increase transmitter release is greatly enhanced by perfusion of the preparation with Ringer solution containing elevated K(+). At concentrations of carbachol greater than 30 muM, the onset of the postjunctional blocking action of carbachol is too rapid and obscures the increase in miniature potential frequency. The rate of increase in transmitter release is dependent on the concentration of carbachol applied and can be antagonized by d-tubocurarine (10-60 nM) and other blocking compounds. These findings, in contrast to previous reports, indicate that cholinergic nerve endings, like adrenergic nerve endings, respond to applied acetylcholine-like drugs with measurable increases in transmitter output.

Acetylcholine↗