If the concentration of intracellular potassium decreases, how would this affect action potential?

The correct answer and explanation is:

Correct Answer:
If the concentration of intracellular potassium decreases, the resting membrane potential becomes less negative (depolarized), and the ability of the neuron to generate and propagate action potentials may be impaired.

Explanation:
The action potential in neurons depends heavily on the concentration gradients of ions, particularly sodium (Na⁺) and potassium (K⁺), across the cell membrane. At rest, the intracellular concentration of potassium is much higher than the extracellular concentration. This difference is maintained by the sodium-potassium pump (Na⁺/K⁺-ATPase), which actively transports K⁺ into the cell and Na⁺ out of the cell.

Potassium ions tend to leak out of the cell through potassium channels, and this movement creates the negative resting membrane potential, typically around -70 mV. The equilibrium potential for potassium, described by the Nernst equation, is a major determinant of the resting membrane potential. When intracellular potassium concentration decreases, the gradient that drives potassium out of the cell is reduced.

As a result, fewer positive charges leave the cell, causing the inside of the neuron to become less negative. This partial depolarization alters the resting potential, making it less stable and closer to the threshold for firing an action potential. However, paradoxically, this can reduce neuronal excitability because the voltage-gated sodium channels, which initiate action potentials, may become inactivated if the membrane potential is chronically depolarized.

Additionally, during the repolarization phase of an action potential, potassium efflux is critical for returning the membrane to its resting potential. If intracellular potassium is low, the repolarization process may be slower or incomplete, leading to abnormal action potential shapes or failed firing altogether.

Therefore, a decrease in intracellular potassium disrupts both the resting potential and the dynamics of action potentials, potentially leading to impaired nerve signaling and neuromuscular symptoms.

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