Which Event Triggers The Creation Of An Action Potential

The creation of an action potential, the fundamental electrical signal of the nervous system, isn't a spontaneous event. It's a carefully orchestrated process triggered by specific events that alter the electrical potential across a neuron's membrane. Understanding these triggers is crucial to comprehending how our brains process information, control movement, and allow us to experience the world.

Resting Membrane Potential: The Starting Point

Before delving into the triggers, it's essential to understand the concept of the resting membrane potential. A neuron at rest maintains a negative electrical potential inside relative to the outside, typically around -70 millivolts (mV). This potential difference is primarily established and maintained by:

Sodium-potassium pump: This active transport protein pumps three sodium ions (Na+) out of the cell for every two potassium ions (K+) it pumps in. This creates a concentration gradient with more Na+ outside and more K+ inside.
Potassium leak channels: These channels allow K+ to leak out of the cell down its concentration gradient. Since the membrane is more permeable to K+ than Na+ at rest, this outward movement of positive charge contributes to the negative resting membrane potential.
Anions inside the cell: Large, negatively charged molecules like proteins and nucleic acids are trapped inside the cell, further contributing to the negative charge.

This resting membrane potential is a state of readiness, a poised trigger waiting for the right stimulus to initiate an action potential.

Depolarization: The Key to Unlocking Action Potentials

The trigger for an action potential is depolarization, a change in the membrane potential towards a more positive value. This happens when positive ions (like Na+) flow into the cell, or negative ions (like Cl-) flow out of the cell. While various stimuli can cause depolarization, the critical threshold for triggering an action potential is typically around -55 mV.

Graded Potentials: Small Steps Towards Threshold

Depolarization often starts with graded potentials. These are small, localized changes in membrane potential that vary in magnitude depending on the strength and duration of the stimulus. Graded potentials can be either:

Excitatory postsynaptic potentials (EPSPs): These are depolarizing graded potentials that make the neuron more likely to fire an action potential. They are often caused by the influx of Na+ or Ca2+ ions.
Inhibitory postsynaptic potentials (IPSPs): These are hyperpolarizing graded potentials (making the membrane potential more negative) that make the neuron less likely to fire an action potential. They are often caused by the influx of Cl- ions or the efflux of K+ ions.

Graded potentials travel passively along the neuron's membrane, decreasing in amplitude as they move away from the site of stimulation. This decay is due to the leakage of ions across the membrane and the electrical resistance of the cytoplasm.

Summation: Adding Up the Stimuli

Whether a neuron reaches the threshold for an action potential depends on the summation of graded potentials. This means that multiple graded potentials, occurring at the same time or in close succession, can add together to reach the threshold. There are two main types of summation:

Temporal summation: This occurs when a single presynaptic neuron fires rapidly, causing a series of EPSPs in the postsynaptic neuron that add up over time. If the EPSPs arrive quickly enough, they can summate before they decay, reaching the threshold for an action potential.
Spatial summation: This occurs when multiple presynaptic neurons fire simultaneously, causing EPSPs at different locations on the postsynaptic neuron. These EPSPs can spread and converge at the axon hillock (the region where the axon originates from the cell body), where they summate.

If the summation of EPSPs is strong enough to overcome any IPSPs and depolarize the membrane potential at the axon hillock to the threshold, an action potential is triggered.

Specific Events That Trigger Depolarization and Action Potentials

Several specific events can trigger depolarization and lead to the creation of an action potential. These events generally involve the opening of ion channels in the neuronal membrane.

1. Neurotransmitter Binding

This is the most common trigger for action potentials in neurons. When an action potential reaches the axon terminal of a presynaptic neuron, it triggers the release of neurotransmitters into the synaptic cleft. These neurotransmitters then diffuse across the cleft and bind to receptors on the postsynaptic neuron.

Ligand-gated ion channels: Many neurotransmitter receptors are ligand-gated ion channels. When a neurotransmitter binds to the receptor, the channel opens, allowing specific ions to flow across the membrane.
- Excitatory neurotransmitters: Neurotransmitters like glutamate and acetylcholine (at nicotinic receptors) bind to receptors that open channels permeable to Na+. The influx of Na+ causes depolarization and an EPSP.
- Inhibitory neurotransmitters: Neurotransmitters like GABA and glycine bind to receptors that open channels permeable to Cl-. The influx of Cl- causes hyperpolarization and an IPSP.

The balance between excitatory and inhibitory neurotransmitter activity determines whether the postsynaptic neuron will reach the threshold for an action potential.

2. Sensory Stimuli

Sensory neurons are specialized to detect various stimuli, such as light, sound, touch, temperature, and chemicals. These stimuli can directly or indirectly open ion channels in the sensory neuron, leading to depolarization.

Mechanoreceptors: These receptors respond to physical deformation, such as pressure or stretch. For example, in the skin, mechanoreceptors open ion channels when the skin is touched, allowing Na+ to enter and depolarize the neuron. In the ear, hair cells deflect in response to sound waves, opening mechanically gated ion channels.
Thermoreceptors: These receptors respond to changes in temperature. Some thermoreceptors open ion channels in response to warmth, while others open them in response to cold.
Photoreceptors: These receptors in the eye respond to light. Light causes a cascade of events that ultimately close Na+ channels in the photoreceptor, leading to hyperpolarization in the dark. When light hits the photoreceptor, the channels close, causing hyperpolarization. The reduction in inhibition then leads to downstream depolarization in other neurons.
Chemoreceptors: These receptors respond to chemicals. For example, taste receptors on the tongue bind to specific chemicals in food, opening ion channels that depolarize the cell. Olfactory receptors in the nose bind to odor molecules, triggering a signaling cascade that opens ion channels.

The depolarization of sensory neurons in response to stimuli generates action potentials that are transmitted to the brain, allowing us to perceive and interpret the world around us.

3. Voltage-Gated Ion Channels (Positive Feedback Loop)

While voltage-gated ion channels are crucial for the propagation of the action potential, they can also contribute to its initiation in certain circumstances.

Initial Depolarization: If a graded potential or other stimulus brings the membrane potential close enough to the threshold, voltage-gated Na+ channels begin to open.
Positive Feedback: The influx of Na+ through these channels further depolarizes the membrane, causing even more voltage-gated Na+ channels to open. This creates a positive feedback loop, where depolarization leads to more depolarization.
Action Potential Triggered: If the positive feedback loop is strong enough, the membrane potential rapidly depolarizes to the peak of the action potential.

This mechanism is particularly important in the axon hillock, where there is a high density of voltage-gated Na+ channels.

4. Artificial Stimulation

Action potentials can also be triggered artificially through direct electrical stimulation of a neuron.

External Electrode: Applying a small electrical current to the neuron through an external electrode can directly depolarize the membrane potential.
Threshold Reached: If the depolarization is strong enough to reach the threshold, an action potential will be triggered.

This technique is used in various research and clinical applications, such as studying neuronal excitability and stimulating muscle contraction.

The Action Potential: A Chain Reaction

Once the membrane potential at the axon hillock reaches the threshold, an action potential is inevitably triggered. This is an "all-or-none" event, meaning that the action potential will occur with the same amplitude and duration regardless of the strength of the stimulus, as long as the threshold is reached.

The action potential consists of several distinct phases:

Depolarization: Voltage-gated Na+ channels open rapidly, allowing a massive influx of Na+ into the cell. This causes the membrane potential to rapidly depolarize to a positive value, typically around +30 mV.
Repolarization: Voltage-gated Na+ channels begin to inactivate, preventing further influx of Na+. At the same time, voltage-gated K+ channels open, allowing K+ to flow out of the cell. The efflux of K+ restores the negative membrane potential, causing repolarization.
Hyperpolarization: The voltage-gated K+ channels remain open for a longer period than necessary to restore the resting membrane potential. This causes the membrane potential to become even more negative than the resting potential, resulting in hyperpolarization.
Return to Resting Potential: The voltage-gated K+ channels eventually close, and the sodium-potassium pump and potassium leak channels restore the membrane potential to its resting value.

Refractory Periods: Limiting Action Potential Frequency

After an action potential, there are two refractory periods that limit the frequency at which a neuron can fire action potentials.

Absolute Refractory Period: During this period, which coincides with the depolarization and repolarization phases of the action potential, it is impossible to trigger another action potential, regardless of the strength of the stimulus. This is because the voltage-gated Na+ channels are either already open or are inactivated.
Relative Refractory Period: During this period, which coincides with the hyperpolarization phase of the action potential, it is possible to trigger another action potential, but only with a stronger-than-normal stimulus. This is because the membrane potential is hyperpolarized, and some of the voltage-gated Na+ channels are still inactivated.

The refractory periods ensure that action potentials travel in one direction down the axon and prevent the neuron from firing excessively.

Factors Affecting Action Potential Triggering

Several factors can affect the likelihood of an action potential being triggered. These include:

Membrane Resistance: Higher membrane resistance means that fewer ions leak out of the cell, making it easier for graded potentials to summate and reach the threshold.
Axon Diameter: Larger axon diameter reduces the internal resistance to current flow, allowing graded potentials to travel further and summate more effectively.
Myelination: Myelination increases the speed of action potential propagation by insulating the axon and preventing ion leakage. This allows graded potentials to travel further and more quickly to the next node of Ranvier, where an action potential can be regenerated.
Drugs and Toxins: Many drugs and toxins can affect the function of ion channels, altering neuronal excitability and affecting the likelihood of action potential triggering.

Clinical Significance

Understanding the events that trigger action potentials is crucial for understanding various neurological disorders. Many diseases and conditions affect the function of ion channels or neurotransmitter receptors, leading to abnormal neuronal excitability and a range of symptoms.

Epilepsy: Epilepsy is a neurological disorder characterized by recurrent seizures. In many cases, seizures are caused by excessive neuronal activity due to abnormal ion channel function or imbalances in excitatory and inhibitory neurotransmitter activity.
Multiple Sclerosis (MS): MS is an autoimmune disease that damages the myelin sheath surrounding nerve fibers. This damage slows down action potential propagation and can lead to a variety of neurological symptoms.
Pain: Chronic pain can be caused by changes in the excitability of sensory neurons, leading to increased action potential firing in response to stimuli that would normally be innocuous.
Anesthesia: Anesthetics work by blocking the function of ion channels, preventing action potentials from being generated and transmitted.

Conclusion

The creation of an action potential is a complex and tightly regulated process that is essential for neuronal communication. It is triggered by specific events that depolarize the neuron's membrane potential to the threshold, typically around -55 mV. These events include neurotransmitter binding to receptors, sensory stimuli, the activity of voltage-gated ion channels, and artificial stimulation. Understanding these triggers and the factors that affect them is crucial for understanding how the nervous system functions and for developing treatments for neurological disorders.