Mechanism of Action
- Alpha-agatoxin - By injecting alpha-agatoxin at the neuromuscular junction the post-junctional glutamate activated channel is blocked and therefore the EJP (Excitatory junctional potential). This will only take place if the synapse is activated during exposure to the toxin. When there already is an EJP it will be reduced rapidly. If the toxin is applied without any synaptical activity there will not be a block. The rate of EJP recovery will be slower when the neurotransmitter glutamate is present.
- Mu-agatoxin - Modifying sodium channels leads to an increased sensitivity of these channels, and so the excitation threshold will be shifted downwards. This results in an elevated probability for sodium channels to open, leading to depolarisation. The calcium influx will take place and because of the increased frequency of spontaneous excitatory postsynaptic currents, neurotransmitter release will take place. Repetitive action potentials of motor neurons will be established.
- Omega-agatoxin - In general ω-agatoxin blocks the presynaptic calcium channels, so that the calcium influx will reduce. This results in a decreased release of neurotransmitter in the synpatic cleft. There are several subtypes which can interfere with each other and make the blocking a dynamic process. When ω-agatoxin-IA and ω-agatoxin-IIA are injected separately, they partially block transmitter release. But when they will be injected together, this leads to a complete block of the EJP.
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