Question

Scorpion toxin triggers an action potential in pain-sensing neurons in animals by binding to a specific receptor. The toxin also acts to delay the inactivation of the neurons voltage-gated Na⁺ channels. Explain how this helps the scorpion better avoid being eaten by an animal.

Short answer

The delay in the inactivation of neurons Na⁺ channels leads to high pain signalling, which helps the scorpion from being eaten by the animal.

Step-by-step solution

Introduction

The venom of the scorpion is a neurotoxic. This has an effect on their pray's neurological system, crippling or killing them. This toxin belongs to the neurotoxic family of complex compounds, which includes a variety of protein complexes with 60-70 cross-linked amino acid groups.

Inactivation of voltage-gated sodium channel

By binding to a particular receptor, the scorpion neurotoxin triggers an action potential in pain-sensing neurons in mammals. Toxins adhere to channels and impede neuronal signalling by blocking voltage-gated channels. The inactivation of voltage-gated sodium channels in neurons is slowed by this toxin. The prolongation of the action potential is caused by the inactivation delayed the channels. Increased pain signalling arises as a result of this. As a result, when a potential predator gets stung by a scorpion, it is more likely to let the scorpion go rather than devour it.

Conclusion

As a result of the scorpion stinging, the potential predator pain signalling is increased.