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Action Potential

Action Potential

Neurons communicate by firing action potentials—the electrochemical signal that is propagated along the axon. The signal results in the release of neurotransmitters at axon terminals, thereby transmitting information to the nervous system. An action potential is a specific "all-or-none" change in membrane potential that results in a rapid spike in voltage.
Membrane potential in neurons
Neurons typically have a resting membrane potential of about -70 millivolts (mV). When they receive...

Action Potential: Phases of Stimulation

Action Potential: Phases of Stimulation

The action potential is a complex electrical event that occurs in excitable cells, such as neurons and muscle cells. It consists of several distinct phases, each with specific characteristics.
Resting Phase:
In this phase, the cell's membrane is at its resting potential, typically around -70 millivolts (mV) for neurons. Inside the cell, there is a higher concentration of potassium ions (K+) and a lower concentration of sodium ions (Na+). Voltage-gated sodium channels are closed, and...

Propagation of Action Potentials

Propagation of Action Potentials

The propagation of an action potential refers to the process by which a nerve impulse, or "action potential," travels along a neuron.
Neurons (nerve cells) have a resting membrane potential, with a slightly negative charge inside compared to outside. This is maintained by ion channels, such as sodium (Na+) and potassium (K+) channels, which control the flow of ions. When a stimulus, like a touch or a signal from another neuron, triggers the neuron, sodium channels open, allowing sodium ions to...

Local Anesthetics: Mechanism of Action

Local Anesthetics: Mechanism of Action

Local anesthetics (LAs) block sensory and motor impulses by inhibiting the sodium channels on the nerve cell membranes. This induces temporary loss of sensation, relieving pain in a specific body area.
Local anesthetics are amphiphilic molecules consisting of a hydrophobic aromatic part linked to a hydrophilic group by an ester or amide linkage. They are weak bases and are usually available as salts, which increases their solubility and stability. Once administered, LAs exist in the body either...

Depolarizing Blockers: Mechanism of Action

Depolarizing Blockers: Mechanism of Action

Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because...

Neuromuscular Junction And Blockade

Neuromuscular Junction And Blockade

The site of chemical communication between a motor neuron and a muscle fiber is called the neuromuscular junction (NMJ). The end of the motor neuron at the NMJ divides into a cluster of synaptic end bulbs. The cytoplasm of these bulbs consists of synaptic vesicles enclosing acetylcholine molecules, the principal neurotransmitter released at the NMJ. The region opposite the synaptic bulb that ends in the muscle fiber is called the motor end plate, which has acetylcholine receptors. Within the...

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Modeling Biological Membranes with Circuit Boards and Measuring Electrical Signals in Axons: Student Laboratory Exercises

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Model Analysis of Post-Stimulation Effect on Axonal Conduction and Block.

Yihua Zhong, Jicheng Wang, Jonathan Beckel

IEEE Transactions on Bio-Medical Engineering

|February 5, 2021

Summary

This study introduces a new model for axonal conduction and block, revealing how ion concentration changes and pumps influence nerve signal transmission during long electrical stimulations. The model explains activity-dependent effects and post-stimulation block mechanisms.

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Area of Science:

Neuroscience
Computational Biology
Biophysics

Background:

Long-duration electrical stimulation's effects on axonal conduction and block are not well understood, despite the clinical use of neurostimulation therapies.
Understanding these effects is crucial for optimizing neurostimulation therapies and predicting outcomes.

Purpose of the Study:

To investigate the role of altered membrane ion concentration gradients and ion pump activity in axonal conduction and block caused by prolonged electrical stimulation.
To develop and utilize a novel computational model for analyzing these phenomena.

Main Methods:

Developed a new model based on Hodgkin-Huxley equations, incorporating changes in sodium (Na+) and potassium (K+) concentrations and ion pump activity.
Employed computer simulations to analyze the effects of long-duration electrical stimulation on unmyelinated axons using the new model.

Main Results:

The model accurately simulates action potential initiation, propagation, and block for short stimulations without significant ion concentration changes.
Successfully replicated activity-dependent effects like action potential attenuation and broadening observed in animal studies.
Simulated axonal block post-long-duration direct current (DC) stimulation, identifying three distinct underlying mechanisms.

Conclusions:

Membrane ion concentrations and pumps are critical factors in post-stimulation and activity-dependent axonal conduction/block.
Stimulation duration significantly impacts axonal response by altering ion concentrations due to applied charges.