The Action of Polymyxin B at the Frog Neuromuscular Junction

Durant, N. N.; Lambert, Jeremy J.

doi:10.1111/j.1476-5381.1981.tb09102.x

Cited by 18 publications

(9 citation statements)

References 26 publications

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“…The concentration-dependent decrease in amplitude of MEPPs in TIMG endplates by the PKC inhibitor PMB confirmed the results of another study that reported a postsynaptic effect of PMB (Durant & Lambert, 1981). PMB also exerted a presynaptic effect, namely an increase of the MEPP frequency.…”

Section: Inhibition Of Pkcsupporting

confidence: 88%

Involvement of protein kinases in the upregulation of acetylcholine release at endplates of alpha‐bungarotoxin‐treated rats.

Plomp

Molenaar

1996

The Journal of Physiology

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1. ACh release from motor nerve endings in diaphragms of rats treated chronically with a-bungarotoxin (a-BuTX) is upregulated at the level of the individual endplate. Involvement of protein kinases in this mechanism of synaptic adaptation was investigated. 2. Miniature endplate potentials (MEPPs) and endplate potentials (EPPs) were recorded after /u-conotoxin treatment, which prevents muscle action potentials. The quantal content at endplates was calculated 'directly', i.e. by dividing the EPP amplitude by the MEPP amplitude. 3. Incubation of muscles from control and a-BuTX-treated rats with H-7, a protein kinase C (PKC) inhibitor, reduced MEPP amplitudes but had no clear effect on quantal contents. Polymyxin B, another PKC inhibitor, had a similar effect on muscles from a-BuTX-treated rats. 4. Incubation of muscles from a-BuTX-treated rats with K252a, a broad-spectrum protein kinase inhibitor of, amongst others, PKC, Ca2P-calmodulin-dependent protein kinase II (CaMKII) and neurotrophin receptor tyrosine kinases, resulted in a 30% decrease of the quantal content. However, K252a did not change the quantal content of controls. Incubations with the closely related compound K252b, which has an exclusively extracellular action, had a similar effect. 5. KN62, a specific inhibitor of CaMKII, decreased the mean quantal content of muscles from a-BuTX-treated rats by 18 %. 6. Tyrphostin 51, a selective tyrosine kinase inhibitor, had no effect on quantal contents of muscles from a-BuTX-treated and control rats. However, it increased the frequency and amplitude of MEPPs in muscles from a-BuTX-treated rats, leaving those of controls unchanged. 7. The extent of reduction of quantal content, caused by K252a, K252b and KN62, varied between endplates of individual muscles from a-BuTX-treated rats; quantal contents at endplates with small MEPPs were more sensitive than those at endplates with large MEPPs. 8. It is concluded that PKC does not play a role in the mechanism of upregulation of ACh release at endplates of a-BuTX-treated rats. Instead, CaMKII and some tyrosine kinases in the presynaptic membrane, as well as in the cytoplasm, might be involved.

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Section: Inhibition Of Pkcsupporting

confidence: 88%

Involvement of protein kinases in the upregulation of acetylcholine release at endplates of alpha‐bungarotoxin‐treated rats.

Plomp

Molenaar

1996

The Journal of Physiology

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“…The effects of PXB at the frog neuromuscular junction have also been studied. PXB is a very potent neuromuscular block whose effects can be partially reversed by addition of calcium (Durant and Lambert, 1981). These studies indicate that PXB influences both structural and physiological properties of the intact cell.…”

mentioning

confidence: 83%

Influence of polymyxin B, a probe for anionic phospholipids, on calcium binding and calcium and potassium fluxes of cultured cardiac cells.

Burt

Duenas

Langer

1983

Circulation Research

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SUMMARY. Polymyxin B, an amphiphilic, cationic peptidolipid, which is thought to bind to anionic phosphohpids in cell membranes, is shown to interact with the cellular calcium of cultured neonatal rat myocardial cells in a dose-dependent, partially reversible manner. At concentrations of less than or equal to 0.1 mM, it has two distinct effects. First, it results in displacement of 1.4 ± 0.3 mmol Ca/kg dry weight, which is equivalent to 18.1 ± 3.4% of the total exchangeable cellular calcium. Total calcium displaced by polymyxin B and a nonspecific cationic probe, lanthanum, at its maximal displacing concentration (1 mM), was 5.9 ±1.3 mmol/kg dry weight. Thus, the total displaceable calcium represented 76.3 ± 2.5% of the total exchangeable calcium. Second, polymyxin B (S0.1 mM) causes a reduction in net uptake of calcium, and slows the efflux of both calcium and potassium. Concentrations of polymyxin B higher than 0.1 mM result in an initial displacement of calcium, followed by an irreversible and sustained period of enhanced net calcium uptake. Efflux of calcium is slowed at the higher polymyxin B concentrations, whereas efflux of potassium is enhanced. Cellular contractile activity and electrical activity are irreversibly altered only by the higher concentrations. The results suggest that polymyxin B is a useful probe for the role of membrane phospholipids in control of ion binding and fluxes. (Circ Res 53: 679-687, 1983)

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“…myasthenia gravis, tubocurarine paralysis). Certainly, 4-aminopyridine seems to be a better antagonist of antibiotics that block transmission predominantly by a prejunctional mechanism (aminoglycosides, polymyxins) than of those that act by a post junctional mechanism (tetracyclines, certain lincosamides) (SOBEK et al 1968;SINGH et al 1978 a, b;LEE et al 1978;MAENO and ENOMOTO 1980;ENOMOTO and MAENO 1981;UCHIYAMA et al 1981;DURANT and LAMBERT 1981). Aminopyridines are also very effective against the depression of transmitter release in experimental botulism LUNDH 1978b;TAZIEFF-DEPIERRE et al 1978;SIMPSON 1978;MOLGO et al 1980), or that produced by crotoxin (VITAL-BRAZIL et al 1979).…”

Section: Repetitive Nerve Stimulationmentioning

confidence: 97%