Picture of boy being examining by doctor at a tuberculosis sanatorium

Understanding our future through Open Access research about our past...

Strathprints makes available scholarly Open Access content by researchers in the Centre for the Social History of Health & Healthcare (CSHHH), based within the School of Humanities, and considered Scotland's leading centre for the history of health and medicine.

Research at CSHHH explores the modern world since 1800 in locations as diverse as the UK, Asia, Africa, North America, and Europe. Areas of specialism include contraception and sexuality; family health and medical services; occupational health and medicine; disability; the history of psychiatry; conflict and warfare; and, drugs, pharmaceuticals and intoxicants.

Explore the Open Access research of the Centre for the Social History of Health and Healthcare. Or explore all of Strathclyde's Open Access research...

Image: Heart of England NHS Foundation Trust. Wellcome Collection - CC-BY.

Strathprints

Effects of charybdotoxin, a blocker of Ca2+-activated K+ channels, on motor nerve terminals

Anderson, A.J. and Harvey, Alan L. and Rowan, E.G. and Strong, P.N. (1988) Effects of charybdotoxin, a blocker of Ca2+-activated K+ channels, on motor nerve terminals. British Journal of Pharmacology, 95 (4). pp. 1329-1335. ISSN 1476-5381

Full text not available in this repository. Request a copy from the Strathclyde author

Abstract

1. The contribution of Ca2+-activated K+ currents (IK,Ca) to the control of electrical excitability of motor nerve terminals and the control of acetylcholine release was assessed by studying the effects of the specific K(Ca) channel blocking toxins charybdotoxin and apamin. Electrical activity of the terminal regions of motor nerves was assessed by extracellular recording from an electrode placed in the perineural sheaths of nerves in the mouse triangularis sterni and frog cutaneous pectoris preparations. Acetylcholine release was monitored by intracellular recording of endplate potentials (e.p.ps). 2. Charybdotoxin (20-300 nM), but not apamin (10 nM-2.5 microM), selectively reduced the amplitude of an IK,Ca unmasked by prior blockade of the delayed rectifier K+ current with 3,4-diaminopyridine (3,4-DAP). 3. In the combined presence of 3,4-DAP and charybdotoxin, large Ca2+-dependent plateau responses developed, but only moderate and transient increases in acetylcholine release occurred. 4. In the absence of 3,4-DAP, charybdotoxin did not alter the electrical activity of, or the transmitter release from motor nerve terminals. 5. A possible role of the charybdotoxin-sensitive IK,Ca in the control of transmitter release is discussed.

Item type: Article
ID code: 18537
Keywords: charybdotoxin, Ca2+-activated K+ channels, motor nerve terminals, Therapeutics. Pharmacology, Pharmacology
Subjects: Medicine > Therapeutics. Pharmacology
Department: Faculty of Science > Strathclyde Institute of Pharmacy and Biomedical Sciences
Depositing user: Dr EG Rowan
Date deposited: 17 Nov 2010 10:05
Last modified: 03 Jan 2019 12:13
Related URLs:
URI: https://strathprints.strath.ac.uk/id/eprint/18537
Export data:
CORE (COnnecting REpositories)