Depolarisation in a nerve action potential is due to:

ESIC Nursing Officer -2019 (Shift -1)

Applied Physiology

Easy

Appeared in: ESIC Nursing Officer -2019 (Shift -1)

Explanation

Depolarization is defined as the phase where the neuron's membrane potential rapidly becomes less negative and eventually positive.
This is caused by the opening of voltage-gated sodium (Na+) channels when the membrane potential reaches a certain threshold.
The opening of these channels allows a large influx of positively charged Na+ ions into the cell, driving the membrane potential up towards the sodium equilibrium potential.
This process creates a positive feedback loop: depolarization opens more Na+ channels, causing further depolarization, which results in the characteristic sharp upstroke of the action potential.

Option B: The opening of calcium channels is not the primary event causing depolarization along the nerve axon. While they play a crucial role, it's typically at the axon terminal.
Option C: The opening of potassium (K+) channels causes the opposite of depolarization; it leads to repolarization.
Option D: Closing of sodium channels is a key part of ending the depolarization phase and starting repolarization. It does not cause depolarization.

Visual 1: Diagram - A labeled graph of a nerve action potential, clearly showing the depolarization, repolarization, and hyperpolarization phases with corresponding ion channel states (Na+ open, K+ open, etc.).
Visual 2: Animation - A dynamic animation showing the lipid bilayer of a neuron with voltage-gated Na+ and K+ channels opening and closing in sequence as an action potential propagates along the axon.

Clinical Relevance

Nursing practice connection: This is primarily an exam-oriented knowledge point with limited direct bedside application, so retain Physiology of Nerve Action Potential as background academic context rather than a clinical decision trigger.
Understanding depolarization is crucial for comprehending how local anesthetics like Lidocaine work. These drugs block voltage-gated sodium channels, preventing depolarization and thus blocking the transmission of pain signals.
Electrolyte imbalances directly affect nerve excitability. For example, hyponatremia (low sodium) can impair depolarization, leading to neurological symptoms like confusion and seizures. Hyperkalemia (high potassium) alters the resting potential, making neurons more excitable initially but can lead to paralysis.
What if? If a patient has a genetic disorder causing sodium channels to inactivate more slowly, the depolarization phase would be prolonged. This could lead to conditions of muscle hyperexcitability, such as myotonia (inability of muscles to relax after contraction).

How to Approach the Question

First, identify the key term in the question: 'Depolarisation'.
Recall the sequence of events in a nerve action potential: resting state -> stimulus -> depolarization -> repolarization -> hyperpolarization -> resting state.
Associate each phase with the primary ion movement responsible for it. For depolarization, this is the 'rising phase'.
Ask yourself: 'What makes the inside of the cell rapidly become positive?' This is the influx of a positive ion.
Evaluate the options: The influx of sodium (Na+) is the well-established cause of the rapid upstroke. Potassium (K+) efflux causes the downstroke (repolarization). Calcium (Ca2+) is mainly for neurotransmitter release. Closing channels would stop the process, not start it.

Concept Tested & Keywords

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