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Sodium channels spider toxins

Turning now to chemical attack, many predators immobilize their prey by injecting toxins, often neurotoxins, into them. Examples include venomous snakes, spiders, and scorpions. Some spider toxins (Quick and Usherwood 1990 Figure 1.3) are neurotoxic through antagonistic action upon glutamate receptors. The venom of some scorpions contains polypeptide neurotoxins that bind to the sodium channel. [Pg.11]

Release of acetylcholine When an action potential propagated by the action of voltage-sensitive sodium channels arrives at a nerve ending, voltage-sensitive calcium channels in the presynaptic membrane open, causing an increase in the concentration of intracellular calcium. Elevated calcium levels promote the fusion of synaptic vesicles with the cell membrane and release of acetylcholine into the synapse. This release is blocked by botulinum toxin. By contrast, black widow spider venom causes all of the cellular acetylcholine stored in synaptic vesicles to spill into the synaptic gap. [Pg.47]

Figure 1. Diagram showing some ion channel targets for venom toxins a generalized insect synaptic junction. Sites 1-3 are presynaptic, 4 is postsynaptic. Site 1 is the insect voltage active sodium channel, targeted by scorpion toxins and spider toxins. Site 2 is the voltage-activated calcium channel. Block of Ms channel invents calcium entry and transmitter release. Site 3 is the latrotoxin receptor, which is involved in the exocytotic release mechanism. Site 4 is the transmitter activated cation channel, which is blocked by acylpolyamine spider toxins. (See Table I for list of toxins acting at these sites). Figure 1. Diagram showing some ion channel targets for venom toxins a generalized insect synaptic junction. Sites 1-3 are presynaptic, 4 is postsynaptic. Site 1 is the insect voltage active sodium channel, targeted by scorpion toxins and spider toxins. Site 2 is the voltage-activated calcium channel. Block of Ms channel invents calcium entry and transmitter release. Site 3 is the latrotoxin receptor, which is involved in the exocytotic release mechanism. Site 4 is the transmitter activated cation channel, which is blocked by acylpolyamine spider toxins. (See Table I for list of toxins acting at these sites).
We concluded that paralysis in insects caused by injection of funnel web spider venom was caused by the joint actions of actions of the a-, p- and -agatoxins, each acting at a distinct ion channel target at the neuromuscular junction. The only toxins showing lethal actions when injected into insects were the p-agatoxins, which also appear to be specific for insect sodium channels. [Pg.255]

Arthropod-derived toxins are also among the list of classical examples of toxins used to probe biochemical processes. Scorpion toxins have been important in the experimental determination of the spacial arrangement of residues on the potassium channel (11), and also in the inference of properties of its quaternary structure (12). A scorpion toxin was used as a tool in the first isolation of a specific component of an insect sodium channel (13). Spider toxins have been similarly useful in characterization of calcium channels (14). [Pg.379]


See other pages where Sodium channels spider toxins is mentioned: [Pg.136]    [Pg.136]    [Pg.401]    [Pg.195]    [Pg.115]    [Pg.363]    [Pg.894]    [Pg.145]    [Pg.249]    [Pg.250]    [Pg.250]    [Pg.255]    [Pg.272]    [Pg.183]   
See also in sourсe #XX -- [ Pg.24 , Pg.287 ]




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