1. The m. triangularis sterni of the mouse was used to investigate the actions of dendrotoxin, beta-bungarotoxin, crotoxin, taipoxin, bee venom phospholipase A2, aprotinin and apamin on presynaptic currents which flow inside the perineural sheath of nerve bundles upon nerve stimulation. 2. Neither the fast K+ current (IK,f) nor the Ca2+-dependent K+ current IK(Ca) (unmasked after blockade of IK,f by 3,4-diaminopyridine) was affected by the neurotoxins and drugs mentioned. 3. Inhibition of both IK,f and IK(Ca) by tetraethylammonium (30 mM) prolonged presynaptic depolarization owing to Ca2+ influx through fast and slow Ca2+ channels. Additional application of dendrotoxin, beta-bungarotoxin, crotoxin or taipoxin in the nanomolar range caused further prolongation of Ca2+ influx, presumably due to blockade of slowly activating K+ current (IK,s). Onset of toxin effects was immediate and could not be reversed by washing for 60 min. 4. Similar prolongation of slow Ca2+ current was effected by 3,4-diaminopyridine, whereas addition of apamin, aprotinin or phospholipase A2 left the signals unchanged. 5. These data indicate that facilitatory actions of dendrotoxin, beta-bungarotoxin, taipoxin and crotoxin are mediated by an increase of Ca2+ entry into nerve terminals. The actions of these toxins are discussed in terms of a blockade of presynaptic K+ channels with slow activation kinetics.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1192472 | PMC |
| http://dx.doi.org/10.1113/jphysiol.1987.sp016544 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Several phospholipase A(2) (PLA(2)) neurotoxins from snake venoms can affect acetylcholine release at the neuromuscular junction. In isolated nerve-muscle preparations three distinct phases have been described for this phenomenon: An initial transient decrease in twitch tension; a second facilitatory phase during which twitch height is greater than control twitch height; and the last phase which causes a reduction in twitch height that finally results in paralysis. Suramin has been reported to inhibit the toxic effects of β-bungarotoxin and another PLA(2) neurotoxin, crotoxin in vitro and in vivo.
View Article and Find Full Text PDFTranscriptomic analysis of the venom gland of the red-headed krait (Bungarus flaviceps) using expressed sequence tags.
BMC Mol Biol
March 2010
Department of Biological Sciences, National University of Singapore, 10 Kent Ridge Road, Singapore 117546, Singapore.
Background: The Red-headed krait (Bungarus flaviceps, Squamata: Serpentes: Elapidae) is a medically important venomous snake that inhabits South-East Asia. Although the venoms of most species of the snake genus Bungarus have been well characterized, a detailed compositional analysis of B. flaviceps is currently lacking.
View Article and Find Full Text PDFThe facilitatory actions of snake venom phospholipase A(2) neurotoxins at the neuromuscular junction are not mediated through voltage-gated K(+) channels.
Toxicon
December 2001
Department of Physiology and Pharmacology, University of Strathclyde, 27 Taylor Street, Glasgow G4 0NR, UK.
Electrophysiological investigations have previously suggested that phospholipase A(2) (PLA(2)) neurotoxins from snake venoms increase the release of acetylcholine (Ach) at the neuromuscular junction by blocking voltage-gated K(+) channels in motor nerve terminals. We have tested some of the most potent presynaptically-acting neurotoxins from snake venoms, namely beta-bungarotoxin (BuTx), taipoxin, notexin, crotoxin, ammodytoxin C and A (Amotx C & A), for effects on several types of cloned voltage-gated K(+) channels (mKv1.1, rKv1.
View Article and Find Full Text PDFBeta-bungarotoxin is a potent inducer of apoptosis in cultured rat neurons by receptor-mediated internalization.
Eur J Neurosci
September 2001
Institut für Biochemie, Emil-Fischer-Zentrum, Universität Erlangen-Nürnberg, Fahrstrasse 17, D-91054 Erlangen, Germany.
The neurotoxic phospholipase A(2), beta-bungarotoxin (beta-BuTx), is a component of the snake venom from the Taiwanese banded krait Bungarus multicinctus. beta-BuTx affects presynaptic nerve terminal function of the neuromuscular junction and induces widespread neuronal cell death throughout the mammalian and avian CNS. To analyse the initial events of beta-BuTx-mediated cell death, the toxin was applied to cultured rat hippocampal neurons where it induced neuronal cell death in a concentration-dependent manner (EC(50) approximately equal to 5 x 10(-13) M) within 24 h.
View Article and Find Full Text PDFWhat does beta-bungarotoxin do at the neuromuscular junction?
Toxicon
January 2001
Department of Physiology and Pharmacology, University of Strathclyde, Strathclyde Institute for Biomedical Sciences, 27 Taylor Street, Glasgow G4 ONR, UK.
beta-Bungarotoxin from the Taiwan banded krait, Bungarus multicinctus is a basic protein (pI=9.5), with a molecular weight of 21,800 consisting of two different polypeptide subunits. A phospholipase A(2) subunit named the A-chain and a non-phospholipase A(2) subunit named the B-chain, which is homologous to Kunitz protease inhibitors.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!