Linked Life Data

9053737

Source:http://linkedlifedata.com/resource/pubmed/id/9053737

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1997-3-7
pubmed:abstractText
Endplate preparations of the rat left hemidiaphragm were incubated with [3H]choline to label neuronal transmitter stores. Nerve evoked release of newly-synthesized [3H]acetylcholine was measured in the absence of cholinesterase inhibitors to investigate whether snake venom neurotoxins by blocking presynaptic nicotinic autoreceptors affect evoked transmitter release. Contractions of the indirectly stimulated hemidiaphragm were recorded to characterize the blocking effect of alpha-neurotoxins at the post-synaptic nicotinic receptors. Neither the long chain neurotoxins alpha-cobratoxin (1 microgram ml-1) and alpha-bungarotoxin (5 microgram ml-1) nor the short chain neurotoxin erabutoxin-b (0.1, 1 and 10 micrograms ml-1) affected the nerve-evoked release of [3H]acetylcholine. kappa-Bungarotoxin (1 and 5 micrograms ml-1), a toxin preferentially blocking neuronal nicotinic receptors, did also not affect evoked [3H]acetylcholine release, whereas (+)-tubocurarine (1 microM) under identical conditions reduced the release by about 50%. alpha-Bungarotoxin, alpha-cobratoxin and erabutoxin-b concentration-dependently (0.01-0.6 micrograms ml-1) inhibited nerve-evoked contractions of the hemidiaphragm. All neurotoxins except erabutoxin-b enhanced the basal tritium efflux immediately when applied to the endplate preparation or to a non-innervated muscle strip labelled with [3H]choline. This effect was attributed to an enhanced efflux of [3H]phosphorylcholine, whereas the efflux of [3H]choline and [3H]acetylcholine was not affected. It is concluded that the alpha-neurotoxins and kappa-bungarotoxin do not block presynaptic nicotinic receptors of motor nerves. These nicotinic autoreceptors differ from nicotinic receptors localized at the muscle membrane and at autonomic ganglia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0028-1298
pubmed:author
pubmed:issnType
Print
pubmed:volume
352
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
646-52
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:9053737-Acetylcholine, pubmed-meshheading:9053737-Animals, pubmed-meshheading:9053737-Bungarotoxins, pubmed-meshheading:9053737-Chromatography, High Pressure Liquid, pubmed-meshheading:9053737-Cobra Neurotoxin Proteins, pubmed-meshheading:9053737-Diaphragm, pubmed-meshheading:9053737-Erabutoxins, pubmed-meshheading:9053737-Female, pubmed-meshheading:9053737-Isotope Labeling, pubmed-meshheading:9053737-Male, pubmed-meshheading:9053737-Muscle, Smooth, pubmed-meshheading:9053737-Muscle Contraction, pubmed-meshheading:9053737-Neurotoxins, pubmed-meshheading:9053737-Phrenic Nerve, pubmed-meshheading:9053737-Rats, pubmed-meshheading:9053737-Receptors, Nicotinic, pubmed-meshheading:9053737-Snake Venoms, pubmed-meshheading:9053737-Synaptic Transmission, pubmed-meshheading:9053737-Tritium
pubmed:year
1995
pubmed:articleTitle
alpha-Bungarotoxin, kappa-bungarotoxin, alpha-cobratoxin and erabutoxin-b do not affect [3H]acetylcholine release from the rat isolated left hemidiaphragm.
pubmed:affiliation
Department of Pharmacology, University of Mainz, Germany.
pubmed:publicationType
Journal Article