Anderson, A J and Harvey, A L (1988) Effects of the potassium channel blocking dendrotoxins on acetylcholine release and motor nerve terminal activity. British Journal of Pharmacology, 93 (1). pp. 215-221. ISSN 1476-5381Full text not available in this repository. (Request a copy from the Strathclyde author)
1. The effects of the K+ channel blocking toxins, the dendrotoxins, on neuromuscular transmission and motor nerve terminal activity were assessed on frog cutaneous pectoris, mouse diaphragm and mouse triangularis sterni nerve-muscle preparations. Endplate potentials (e.p.ps) and miniature e.p.ps were recorded with intracellular microelectrodes, and nerve terminal spikes were recorded with extracellular electrodes placed in the perineural sheaths of motor nerves. 2. Dendrotoxin from green mamba (Dendroaspis angusticeps) venom and toxin I from black mamba (D. polylepis) venom increased the amplitude of e.p.ps by increasing quantal content, and also induced repetitive e.p.ps. 3. Perineural recordings revealed that dendrotoxins could decrease the component of the waveform associated with K+ currents at the nerve terminals, and induce repetitive activation of nerve terminals. 4. In frog motor nerves, dendrotoxins are known to block the fast f1 component of the K+ current at nodes of Ranvier. Blockade of a similar component of the K+ current at motor nerve terminals may be responsible for the effects of these toxins on neuromuscular transmission. 5. Similar conclusions can be drawn from the results obtained from mouse neuromuscular junctions.
|Keywords:||acetylcholine, animals, elapid venoms, ion channels, male, mice, inbred BALB C mice, motor endplate, nerve endings, neurotransmitter agents, rana pipiens, rana temporaria, respiratory muscles, Pharmacy and materia medica, Pharmacology|
|Subjects:||Medicine > Pharmacy and materia medica|
|Department:||Faculty of Science > Strathclyde Institute of Pharmacy and Biomedical Sciences|
|Depositing user:||Pure Administrator|
|Date Deposited:||13 Jul 2011 08:57|
|Last modified:||03 Feb 2017 12:26|