Action Potential Overview and Mechanisms

Action potentials (APs) are rapid, all-or-none electrical signals that travel down the axon of a neuron. They are essential for rapid communication between neurons and other cells.

Action potentials are generated when a neuron reaches its threshold voltage, causing voltage-gated sodium channels to open and sodium ions to rush into the cell.

The rising phase of an action potential is characterized by a rapid depolarization of the membrane, as sodium ions flow into the cell. This phase is driven by the opening of voltage-gated sodium channels.

The falling phase of an action potential is characterized by a rapid repolarization of the membrane, as potassium ions flow out of the cell. This phase is driven by the closing of sodium channels and the opening of voltage-gated potassium channels.

The absolute refractory period is a brief period after an action potential during which it is impossible for another action potential to be generated. This is because sodium channels remain inactivated.

The relative refractory period is a period after the absolute refractory period during which it is harder to generate another action potential. This is because sodium channels are recovering and the membrane is still hyperpolarized.

The frequency of action potentials in an axon is determined by the intensity of the stimulus. Stronger stimuli lead to higher frequencies of action potentials.

The number of axons firing action potentials is determined by the strength of the stimulus. Stronger stimuli lead to more axons being activated.

A narrow region within an ion channel that determines which ions can pass through.

The transmembrane segment of a voltage-gated ion channel that senses changes in membrane potential. Positively charged amino acid residues in this segment move outward in response to depolarization, opening the pore.

Regions within the S5 and S6 segments of a voltage-gated ion channel that fold into the pore and are responsible for ion selectivity.

A cytoplasmic domain of a voltage-gated ion channel that blocks the pore from the inside, leading to inactivation of the channel.

The ability of a membrane to conduct electrical signals passively, without active involvement of ion channels.

The distance along an axon or dendrite where an initial voltage change decays to 37% of its original value. It reflects the spread of depolarization.

The time it takes for an initial voltage change to decay to 37% of its original value. It reflects how long depolarization lasts.

The propagation of an action potential along an axon, starting at the axon hillock and ending at the axon terminal.

Hodgkin and Huxley's groundbreaking research on the squid giant axon, which involved recording action potentials and identifying the ionic currents responsible for them. They proposed the concept of voltage-dependent "gating particles" that control ion flow across the membrane.

The initial phase of an action potential, where the membrane potential rapidly rises from negative to positive values. This is primarily driven by the influx of sodium ions into the cell.

The peak of an action potential where the membrane potential reaches a maximum value, often overshooting the resting potential. This is attributed to the continued influx of sodium ions until the sodium channels close.

The phase of an action potential following the overshoot where the membrane potential rapidly decreases back towards its resting value. This is mainly due to the outward flow of potassium ions leaving the cell.

The period after the action potential when the membrane potential falls below the resting potential. This is caused by the continued outward flow of potassium ions and the slow recovery of the membrane.

The difference in electrical charge across the cell membrane when the cell is not actively signaling. It is typically maintained by the balance of ion gradients and the permeability of the membrane to different ions.

The hypothesis that the influx of sodium ions through voltage-gated sodium channels is responsible for the rising and overshoot phases of an action potential. This is a key concept in understanding how the action potential is generated.

The movement of ions across the cell membrane through specific channels that open or close in response to changes in membrane potential. This mechanism underlies the rapid changes in membrane permeability during an action potential.

A change in membrane potential that triggers the opening of sodium channels, leading to a rapid influx of Na+ ions and further depolarization.

A specific type of ion channel protein responsible for the rapid influx of sodium ions (Na+) during an action potential.

A specific type of ion channel protein responsible for the outward flow of potassium ions (K+) during an action potential.

The process where the activation gate (M) of the sodium channel opens, increasing sodium permeability and causing further depolarization.

The process where the inactivation gate (H) of the sodium channel closes, decreasing sodium permeability and initiating repolarization.

The process where the potassium channel (N) opens, increasing potassium permeability and contributing to repolarization.

The region of the ion channel protein responsible for sensing changes in membrane voltage and initiating gate opening.

The sequence of events involving the opening and closing of sodium and potassium channels during an action potential, leading to the rapid depolarization and subsequent repolarization of the nerve cell membrane.

Voltage-dependent channels are specialized proteins embedded in the cell membrane that open or close in response to changes in membrane potential. They play a crucial role in the propagation of action potentials, allowing for the rapid transmission of signals along neurons.

The inactivation of voltage-dependent channels limits the frequency of action potentials that can be generated. This is because after an action potential, the channels need time to reset before they can be activated again.

Myelin is a fatty substance that wraps around axons, providing insulation and increasing the length constant. This allows for faster and more efficient conduction of action potentials.

Saltatory conduction is the process of action potential propagation along myelinated axons, where the signal 'jumps' from one node of Ranvier to the next. This allows for faster transmission of information down the axon.

Nodes of Ranvier are gaps in the myelin sheath where voltage-dependent channels are concentrated. These gaps are essential for the propagation of action potentials as they allow for the generation of new signals.

Action potential conduction velocity is the speed at which an action potential travels along an axon. It is affected by factors such as the presence of myelin and the diameter of the axon.

Increasing the resistance across the membrane (RM) and decreasing the resistance of the cytoplasm (RA) both contribute to increasing the length constant, leading to faster action potential conduction. This is achieved through myelination and having larger diameter axons.