Abstract
| Language | English |
|---|---|
| Pages | 1871-1882 |
| Number of pages | 11 |
| Journal | Toxicon |
| Volume | 39 |
| Issue number | 12 |
| DOIs | |
| Publication status | Published - Dec 2001 |
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Keywords
- beta-bungarotoxin
- taipoxin
- notexin
- crotoxin
- ammodytoxin
- phospholipase A(2)
- voltage-gated K+ channels
- neuromuscular junction
- acetylcholine release
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The facilitatory actions of snake venom phospholipase a(2) neurotoxins at the neuromuscular junction are not mediated through voltage-gated k+ channels. / Fathi, B.; Rowan, E.G.; Harvey, A.L.
In: Toxicon, Vol. 39, No. 12, 12.2001, p. 1871-1882.Research output: Contribution to journal › Article
TY - JOUR
T1 - The facilitatory actions of snake venom phospholipase a(2) neurotoxins at the neuromuscular junction are not mediated through voltage-gated k+ channels
AU - Fathi, B.
AU - Rowan, E.G.
AU - Harvey, A.L.
PY - 2001/12
Y1 - 2001/12
N2 - Electrophysiological investigations have previously suggested that phospholipase A2 (PLA2) 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 β-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, rKv1.2, mKv1.3, hKv1.5 and mKv3.1) stably expressed in mammalian cell lines. By use of the whole-cell configuration of the patch clamp recording technique and concentrations of toxins greater than those required to affect acetylcholine release, these neurotoxins have been shown not to block any of these voltage-gated K+ channels. In addition, internal perfusion of the neurotoxins (100 μg/ml) into mouse B82 fibroblast cells that expressed rKv1.2 channels also did not substantially depress K+ currents. The results of this study suggest that the mechanism by which these neurotoxins increase the release of acetylcholine at the neuromuscular junction is not related to the direct blockage of voltage-activated Kv1.1, Kv1.2, Kv1.3, Kv1.5 and Kv3.1 K+ channels.
AB - Electrophysiological investigations have previously suggested that phospholipase A2 (PLA2) 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 β-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, rKv1.2, mKv1.3, hKv1.5 and mKv3.1) stably expressed in mammalian cell lines. By use of the whole-cell configuration of the patch clamp recording technique and concentrations of toxins greater than those required to affect acetylcholine release, these neurotoxins have been shown not to block any of these voltage-gated K+ channels. In addition, internal perfusion of the neurotoxins (100 μg/ml) into mouse B82 fibroblast cells that expressed rKv1.2 channels also did not substantially depress K+ currents. The results of this study suggest that the mechanism by which these neurotoxins increase the release of acetylcholine at the neuromuscular junction is not related to the direct blockage of voltage-activated Kv1.1, Kv1.2, Kv1.3, Kv1.5 and Kv3.1 K+ channels.
KW - beta-bungarotoxin
KW - taipoxin
KW - notexin
KW - crotoxin
KW - ammodytoxin
KW - phospholipase A(2)
KW - voltage-gated K+ channels
KW - neuromuscular junction
KW - acetylcholine release
UR - http://dx.doi.org/10.1016/S0041-0101(01)00170-2
U2 - 10.1016/S0041-0101(01)00170-2
DO - 10.1016/S0041-0101(01)00170-2
M3 - Article
VL - 39
SP - 1871
EP - 1882
JO - Toxicon
T2 - Toxicon
JF - Toxicon
SN - 0041-0101
IS - 12
ER -