Abstract
β-Bungarotoxin and crotoxin are phospholipase A2 neurotoxins, which block irreversibly the evoked release of acetylcholine from motor nerve terminals of mouse triangularis sterni preperations. Extracellular recording of nerve terminal action potentials reveal that inhibition of transmitter release is not associated with failure of the action potential to invade nerve terminals. When evoked transmitter release (measured as intracellularly recorded endplate potentials) was blocked by β-bungarotoxin, spontaneous acetylcholine release was stimulated as in control experiments by K+-induced depolarization and by the Ca2+-ionophore A23187. The site of action of the toxins remains to be elucidated but would appear to be associated with the coupling of action potential induced-depolarization to the release mechanism, rather than with the release mechanism itself.
| Original language | English |
|---|---|
| Pages (from-to) | 301-304 |
| Number of pages | 4 |
| Journal | British Journal of Pharmacology |
| Volume | 100 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 1 Jan 1990 |
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Keywords
- beta bungarotoxin
- calcimycin
- crotoxin
- potassium ion
- snake venom
- tubocurarine chloride
- acetylcholine release
- action potential
- nerve ending
- neuromuscular synapse
Cite this
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On the blockade of acetylcholine release at mouse motor nerve terminals by β-bungarotoxin and crotoxin. / Rowan, E. G.; Pemberton, K. E.; Harvey, A. L.
In: British Journal of Pharmacology, Vol. 100, No. 2, 01.01.1990, p. 301-304.Research output: Contribution to journal › Article
TY - JOUR
T1 - On the blockade of acetylcholine release at mouse motor nerve terminals by β-bungarotoxin and crotoxin
AU - Rowan, E. G.
AU - Pemberton, K. E.
AU - Harvey, A. L.
PY - 1990/1/1
Y1 - 1990/1/1
N2 - β-Bungarotoxin and crotoxin are phospholipase A2 neurotoxins, which block irreversibly the evoked release of acetylcholine from motor nerve terminals of mouse triangularis sterni preperations. Extracellular recording of nerve terminal action potentials reveal that inhibition of transmitter release is not associated with failure of the action potential to invade nerve terminals. When evoked transmitter release (measured as intracellularly recorded endplate potentials) was blocked by β-bungarotoxin, spontaneous acetylcholine release was stimulated as in control experiments by K+-induced depolarization and by the Ca2+-ionophore A23187. The site of action of the toxins remains to be elucidated but would appear to be associated with the coupling of action potential induced-depolarization to the release mechanism, rather than with the release mechanism itself.
AB - β-Bungarotoxin and crotoxin are phospholipase A2 neurotoxins, which block irreversibly the evoked release of acetylcholine from motor nerve terminals of mouse triangularis sterni preperations. Extracellular recording of nerve terminal action potentials reveal that inhibition of transmitter release is not associated with failure of the action potential to invade nerve terminals. When evoked transmitter release (measured as intracellularly recorded endplate potentials) was blocked by β-bungarotoxin, spontaneous acetylcholine release was stimulated as in control experiments by K+-induced depolarization and by the Ca2+-ionophore A23187. The site of action of the toxins remains to be elucidated but would appear to be associated with the coupling of action potential induced-depolarization to the release mechanism, rather than with the release mechanism itself.
KW - beta bungarotoxin
KW - calcimycin
KW - crotoxin
KW - potassium ion
KW - snake venom
KW - tubocurarine chloride
KW - acetylcholine release
KW - action potential
KW - nerve ending
KW - neuromuscular synapse
UR - http://www.scopus.com/inward/record.url?scp=0025300690&partnerID=8YFLogxK
U2 - 10.1111/j.1476-5381.1990.tb15799.x
DO - 10.1111/j.1476-5381.1990.tb15799.x
M3 - Article
VL - 100
SP - 301
EP - 304
JO - British Journal of Pharmacology
JF - British Journal of Pharmacology
SN - 0007-1188
IS - 2
ER -