Channel Kinetics and the Ionic Basis of the Spike
In a typical sodium-based neuronal action potential, sodium channels open rapidly and then inactivate, while delayed potassium channels open more slowly. Voltage-clamp recordings and tests that isolate ionic currents reveal these different timings.
What a learner can do afterwards
- Assigns each phase of the spike to the channel population responsible.
- Distinguishes closed-available sodium channels from inactivated ones, and explains absolute and relative refractory periods.
- Explains what voltage-clamp current reveals and why additional tests are needed to distinguish ionic currents.
1 · Read
You have linked resting voltage to ion gradients and permeability. In a typical sodium-based neuronal action potential, or spike, sodium channels open rapidly and sodium entry drives the rise. Sodium channels then inactivate as delayed potassium channels open. Potassium exit drives repolarization, the fall. These events overlap. Potassium channels can stay open after the fall, pulling voltage below rest toward potassium's equilibrium value.
Threshold marks the start of a self-amplifying rise. Sodium entry depolarizes the membrane, opening more available sodium channels and allowing more sodium entry. Below threshold, this feedback is too weak to sustain a spike. Under the same conditions, reaching threshold triggers an all-or-none spike. A stronger input does not produce a proportionally taller spike.
A closed-available sodium channel passes no sodium but can open with depolarization. An inactivated channel also passes no sodium and must recover first. Repolarization allows recovery. In the absolute refractory period, channel availability is too low for another spike, even with a strong stimulus. In the relative period, enough channels have recovered to allow a spike, but remaining inactivation and elevated potassium conductance mean a stronger stimulus is usually needed.
A voltage clamp injects current to hold a chosen membrane voltage. Once membrane-charging current is accounted for, the injected current balances the net ionic current. A depolarizing step below sodium's equilibrium voltage but above potassium's can show early inward current and delayed outward current. Selective blockers or ion changes help identify the components. Voltage clamp alone does not separate them.
Suppose a blocker reduces delayed potassium current while sodium-channel function and ion gradients stay unchanged. Less positive charge leaves through those potassium channels, so repolarization is slower. The spike can last longer, and its undershoot may also change. Blocking one channel type need not affect only one phase, because channel activity overlaps.
Sodium entry drives the rise. Sodium inactivation and delayed potassium exit drive the fall. Channel recovery and potassium conductance shape the refractory periods.
Original lesson, questions and flashcards written for this dataset.
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Following the currents through a spike
The resting-voltage lesson explained how gradients and permeability affect membrane voltage. During a typical sodium-based neuronal spike, voltage-gated channels change permeability over a short time.
Sodium channels open rapidly when the membrane depolarizes. While membrane voltage is below sodium's equilibrium value, open sodium channels carry net sodium entry. This brings positive charge inward and drives the rising phase.
Sodium channels then inactivate, reducing sodium entry. Delayed potassium channels open more slowly. Because membrane voltage is above potassium's equilibrium value during the falling phase, potassium leaves through these channels. Losing positive charge brings voltage downward.
These channel activities overlap. Potassium channels may remain open after voltage passes the resting level, producing an undershoot called afterhyperpolarization. Ion pumps maintain the gradients over time; a pump does not reverse direction to create each phase.
What changes at threshold?
Opening a few sodium channels does not always start a spike. A small voltage change can fade before it recruits enough further channel opening.
At threshold, sodium-channel feedback can sustain the rise. Sodium enters, the membrane depolarizes further, and more available sodium channels open. Their current produces further depolarization. This repeating process drives the rapid upstroke.
All-or-none describes the triggering of this regenerative event under the same conditions. It does not mean every neuron has the same waveform. Channel availability, ion gradients and drugs can change the waveform or prevent a spike. A larger stimulus also does not produce a proportionally taller spike in an otherwise unchanged neuron.
Along an axon and across a synapse
Current from an active axon region spreads to nearby membrane. If the nearby membrane reaches threshold, its own voltage-gated channels generate a local action potential. Repeating this process carries the signal along the axon.
Myelin changes where regeneration occurs. Current spreads through the insulated regions, and action potentials are regenerated at gaps called nodes of Ranvier. This pattern is called saltatory conduction. The apparent jump is between nodes on the same axon.
An action potential does not jump directly across a chemical synapse into the next cell. At the terminal, the arriving spike triggers events that release neurotransmitter. Receptors on the receiving cell produce a separate electrical response. That cell fires an action potential only if its own conditions for firing are met.
When another spike becomes possible
A channel can stop conducting sodium in more than one state. A closed-available channel can open with depolarization. An inactivated channel cannot do so until it has recovered. Repolarization permits that recovery.
During the absolute refractory period, sodium-channel availability is too low to support another regenerative spike. Increasing stimulus strength cannot make the neuron fire a second spike at that stage.
Recovery is gradual. In the relative refractory period, another spike becomes possible, but the neuron is less excitable than usual. Some sodium channels remain unavailable, and elevated potassium conductance opposes depolarization. A stronger stimulus is usually required.
These periods help limit firing frequency. Calling both periods a complete inability to respond would miss the distinction between them.
Travel speed is different from firing frequency
Conduction speed measures how fast an action potential travels along an axon. Firing frequency measures how many action potentials occur per unit time. A statement about one does not directly answer a question about the other.
Axon diameter and myelin affect conduction speed. A larger diameter lowers resistance to current flowing along the axon. Myelin reduces current leakage and membrane capacitance in covered regions, helping nearby excitable membrane reach threshold sooner.
Sodium-channel recovery affects when a membrane region can generate another spike. This limits how often that region can fire. It does not impose the same numerical limit on how quickly a spike travels. Several spikes can be present at different positions along a long axon while each local region follows its own recovery cycle.
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