The Resting Potential and the Action Potential
A neurone's resting voltage depends mainly on ion gradients and its greater permeability to potassium. An ATP-driven pump maintains the gradients. During an action potential, voltage-gated sodium and potassium channels change the voltage in sequence.
What a learner can do afterwards
- Explains what maintains the resting potential and what it costs the cell.
- Orders depolarisation, repolarisation and hyperpolarisation and matches them to the rise, fall and dip below resting voltage.
- Says which ion moves at each stage and through which kind of channel.
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A typical neurone rests near minus 70 millivolts (mV), measured inside relative to outside. Values vary. The membrane is more permeable to potassium than sodium. Some potassium leaves through leak channels, separating charge and making the inside negative. The resulting voltage opposes further potassium loss. This permeability, together with ion gradients, is the main basis of the resting potential.
As in co-transport, the sodium potassium pump maintains ion gradients. It uses one ATP per cycle to move three sodium ions out and two potassium ions in. The pump also contributes directly to voltage, but mainly supports resting voltage by maintaining gradients. Blocking it does not erase existing gradients at once. Continued ion movement weakens them over time, so resting voltage tends to become less negative.
If depolarisation reaches threshold, an action potential begins. Voltage-gated sodium channels open rapidly. Sodium enters and voltage rises: depolarisation. Sodium channels then inactivate while slower voltage-gated potassium channels open. Potassium leaves and voltage falls: repolarisation. Continued potassium outflow can briefly take voltage below the resting level: hyperpolarisation.
The dip occurs because voltage-gated potassium channels close slowly, allowing potassium to keep leaving briefly. As these channels close, the usual resting ion conductances bring voltage back toward rest. The pump maintains concentrations over time; it does not directly cause the rapid fall or end the dip. A typical spike lasts a few milliseconds, though timing varies.
An impulse normally travels along an axon as local electrical current brings the next region to threshold. Voltage-gated sodium channels there open and generate another action potential. Just behind it, recently used sodium channels are temporarily inactivated. This refractory region cannot immediately fire again, limiting backward re-excitation. The pump keeps maintaining gradients throughout.
Small local voltage changes can fade with distance. Reaching threshold triggers a full, all-or-nothing spike. Under the same conditions, a stronger stimulus does not produce a proportionally larger spike. Chemical synapses can start local changes through neurotransmitter-gated channels; sensory signals can start through other channels. Myelin, axon diameter and the distribution of voltage-gated channels affect conduction speed.
The pump maintains ion gradients. Potassium permeability mainly shapes resting voltage. Sodium entry drives the spike's rise; potassium exit drives its fall and brief dip.
Lesson, questions and flashcards written for this dataset.
Readings and flashcards written for this dataset. Linked videos by Khan Academy.
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Why the resting voltage is negative
A voltage measurement needs a reference. For membrane potential, the outside is the reference and the value describes the inside relative to it. Minus 70 mV is a common resting example, but values differ between neurones.
Potassium is more concentrated inside. The resting membrane is more permeable to potassium than sodium, so potassium movement through leak channels strongly affects voltage. A small outward movement of potassium separates charge. The negative voltage that develops opposes further potassium loss. Most potassium remains inside.
The sodium potassium pump keeps the concentration differences from running down. Each cycle uses one ATP to move three sodium ions out and two potassium ions in. This also contributes directly to voltage, but selective permeability and ion gradients explain most of the resting potential.
If the pump stops, the existing gradients do not disappear immediately. They weaken as ion movement continues without pumping to maintain them.
Reading the rise, fall and dip
An action-potential trace plots membrane voltage against time. Find the resting level before interpreting the changes.
During the rapid rise, voltage-gated sodium channels open and sodium enters. This depolarisation can make the inside positive relative to outside. Sodium channels then inactivate while slower voltage-gated potassium channels open. Potassium leaves, carrying positive charge out. Voltage falls toward rest in repolarisation.
Potassium channels can remain open briefly after voltage reaches the resting level. Further potassium outflow then produces hyperpolarisation, a dip below resting voltage.
As these channels close, the normal resting conductances bring voltage back toward rest. The sodium potassium pump continues maintaining ion concentrations. It does not directly drive the fast falling phase or act as a switch that ends the dip.
A typical spike lasts a few milliseconds. Exact voltages and timings depend on the neurone and conditions.
How the next axon region fires
A local voltage change does not always produce an impulse. Small changes can fade with distance. If depolarisation reaches threshold, voltage-gated sodium channels generate an action potential. Under the same conditions, a stronger stimulus does not produce a proportionally larger spike: the response is all-or-nothing.
Current from an active region spreads locally and brings the next axon region to threshold. That region generates its own action potential. The recently active region behind it has temporarily inactivated sodium channels. This refractory state limits immediate backward re-excitation.
Chemical synapses can produce local voltage changes when neurotransmitter affects channels. Sensory signals can begin through other mechanisms, such as mechanically gated channels. Chemical gating is not the start of every neuronal signal.
Myelin reduces current leakage, while action potentials are regenerated at gaps called nodes. Axon diameter and channel distribution also affect conduction. Pumps maintain the ion gradients throughout this activity.
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