Certain species of frogs in the genus Phyllobates have a powerful defensive adaptation—their skin can secrete a milky fluid that contains an extremely toxic compound called batrachotoxin (BTX). These frogs, which are found in Colombia, are known as poison dart frogs because some indigenous Colombian hunters coat the tips of their blowgun darts with the frogs' skin secretions. An animal hit by one of these darts dies quickly.
What is the mechanism of action of BTX?
Predict the effects of each of the following on the membrane potential of a neuron simultaneously poisoned with BTX:
(a) Removing extracellular sodium ions;
(b) Increasing the intracellular potassium ion concentration;
(c) Adding tetrodotoxin from puffer fish.

Verified step by step guidance

1. Batrachotoxin (BTX) is a potent toxin that affects the nervous system by binding to voltage-gated sodium channels in neurons. This binding keeps the sodium channels open, preventing them from closing, which leads to a continuous influx of sodium ions into the neuron.
2. To predict the effects of removing extracellular sodium ions on a neuron poisoned with BTX, consider that BTX keeps sodium channels open. If extracellular sodium ions are removed, the gradient driving sodium into the cell is reduced, potentially decreasing the depolarization effect caused by BTX.
3. Increasing the intracellular potassium ion concentration affects the membrane potential by altering the potassium gradient. Normally, potassium ions flow out of the neuron, contributing to repolarization. Increasing intracellular potassium reduces this gradient, potentially making repolarization less effective and maintaining a depolarized state.
4. Tetrodotoxin (TTX) from puffer fish is known to block voltage-gated sodium channels. If TTX is added to a neuron poisoned with BTX, it could counteract BTX's effect by preventing sodium channels from opening, thus reducing sodium influx and potentially restoring normal membrane potential.
5. Consider the combined effects of these manipulations on the membrane potential: removing extracellular sodium ions reduces depolarization, increasing intracellular potassium affects repolarization, and adding TTX blocks sodium channels. Together, these actions could counteract the continuous depolarization caused by BTX, potentially stabilizing the membrane potential.

Key Concepts

Batrachotoxin Mechanism of Action

Batrachotoxin (BTX) is a potent neurotoxin that affects the function of voltage-gated sodium channels in neurons. It binds to these channels, forcing them to remain open, which disrupts the normal flow of sodium ions into the cell. This leads to a continuous depolarization of the neuron, preventing it from returning to its resting state and causing paralysis or death due to uncontrolled nerve signaling.

Membrane Potential

Membrane potential refers to the electrical potential difference across a cell's plasma membrane, primarily influenced by the distribution of ions like sodium, potassium, and chloride. In neurons, the membrane potential is crucial for the generation and propagation of action potentials. Changes in ion concentrations inside or outside the cell can significantly alter the membrane potential, affecting neuronal excitability and signaling.

Tetrodotoxin and Ion Channel Blockage

Tetrodotoxin (TTX) is another neurotoxin that specifically blocks voltage-gated sodium channels, preventing sodium ions from entering the neuron. This blockage inhibits action potential generation, leading to a loss of nerve signal transmission. When applied to a neuron poisoned with BTX, TTX can counteract BTX's effects by preventing the continuous influx of sodium ions, potentially stabilizing the membrane potential and reducing toxicity.