Crayfish giant axons, action

The neurotoxic actions of T17 on membrane excitability were examined in squid giant axon initially and in more detail using crayfish giant axon and intracellular microelectrode techniques(14). Detailed studies utilizing T34 are not available due to technical problems associated with its extreme hydrophobicity and resulting diffi-... 

Figure I. Action Potentials from crayfish giant axons. Control = Top Trace. Toxin (0.8 ug/ml) reduced rise rate and amplitude after 3, 10, 15, 20, and 25 min.

In squid giant axons, PbTx causes a depolarization of the plasma membrane, repetitive discharges followed by depression of action potentials, and a complete blockade of excitability. This action is antagonized by TTX (83,84). PbTx depolarizes nerve terminals and induces neurotransmitter release (85,86) it depolarizes skeletal muscle cells (87) and increases the frequency of action potentials in crayfish nerve cord (88). PbTx also produces a contraction of the guinea pig ileum (89). All these effects are prevented by TTX. 

A species of sea anemone, Condylactis gigantia, produces a polypeptide toxin of unknown structure and molecular weight of around 13 000 which affects the kinetics of some sodium channels. In the giant axon of the crayfish (but not of the squid) condylactis toxin prolongs the falling phase of the action potential by delaying the inactivation of the transient sodium current, without pronounced effect on the steady-state potassium current [136]. 

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