Excitation Contraction Uncoupling
Excitation Contraction Uncoupling - Related Videos
08:29
Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling
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Cited by 9 •
2016
This paper describes a protocol that assesses the changes of myofilament Ca2+ sensitivity during contraction in isolated cardiac myocytes from rat heart. Together with cardiac electrophysiology, systolic/diastolic cytosol Ca2+ levels and contraction/relaxation, this measurement is imperative in underpinning the mechanisms mediating cardiac excitation-contraction coupling in healthy and diseased hearts.
01:20
Excitation-Contraction Coupling in Skeletal Muscles
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2025
Excitation-contraction coupling is a series of events that occur between generating an action potential and initiating a muscle contraction. It occurs at the triad, a structure found in skeletal muscle fibers that comprise a T-tubule and terminal cisternae of the sarcoplasmic reticulum on each side. These triads are visible in longitudinally sectioned muscle fibers. They are typically located at the A-I junction — the junction between the A and I bands of the sarcomere. When an action potential...
12:13
Assessing Primary Motor Cortex Excitability and Excitability Modulation by Pairing Transcranial Magnetic Stimulation with Electromyography
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2025
Here, we present a protocol outlining the methodology to assess primary motor cortex excitability and excitability modulation using transcranial magnetic stimulation (TMS) paired with electromyography (EMG).
01:15
Muscle Contraction
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2025
In skeletal muscles, acetylcholine is released by nerve terminals at the motor end plate—the point of synaptic communication between motor neurons and muscle fibers. Binding of acetylcholine to its receptors on the sarcolemma allows entry of sodium ions into the cell and triggers an action potential in the muscle cell. Thus, electrical signals from the brain are transmitted to the muscle. Subsequently, the enzyme acetylcholinesterase breaks down acetylcholine to prevent excessive muscle...
01:10
Muscle Contraction
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2023
In skeletal muscles, acetylcholine is released by nerve terminals at the motor endplate—the point of synaptic communication between motor neurons and muscle fibers. The binding of acetylcholine to its receptors on the sarcolemma allows entry of sodium ions into the cell and triggers an action potential in the muscle cell. Thus, electrical signals from the brain are transmitted to the muscle. Subsequently, the enzyme acetylcholinesterase breaks down acetylcholine to prevent excessive muscle...
FAQs
Failure may occur at several linked stages: depolarization may not effectively activate voltage-sensitive dihydropyridine receptors, receptor signaling may not trigger ryanodine receptor-mediated calcium release, or released calcium may not support normal activation of the contractile apparatus. Separating these possibilities helps identify whether the defect lies in membrane signaling, calcium handling, or mechanical force generation.
Inadequate calcium release limits the calcium signal available after electrical stimulation. Impaired calcium sensitivity means the contractile machinery responds poorly even when calcium is present. These mechanisms can both reduce force, but they represent different points of failure. Distinguishing them is important when interpreting electrically stimulated muscle assays or evaluating engineered tissue performance.
A muscle cell can receive an action potential and still produce little force if sarcomere function is disrupted. Sarcomeres contain the actin-myosin machinery responsible for mechanical output, so defects downstream of calcium activation can prevent appropriate contraction. This distinction prevents electrical responsiveness from being mistaken for intact muscle function in bioengineered constructs.
A typical investigation electrically stimulates the engineered tissue and compares the resulting force production with the applied excitation. Interpreting the response requires considering the signaling sequence from depolarization through calcium release, calcium activation, and sarcomere action. A reduced or distorted force response can then be analyzed according to which stage of this sequence may be compromised.
The system should relate electrical stimulation to the mechanical response rather than treating excitation alone as the outcome. Force production provides the key functional readout, while the response pattern can indicate whether stimulation leads to appropriate contraction. This pairing allows engineers to evaluate how effectively a cardiac or skeletal muscle construct converts an electrical input into mechanical output.
Excitation contraction uncoupling provides a framework for testing engineered muscle tissues and in vitro models under conditions relevant to disease, toxicity, and drug responses. It also supports assessment of cardiac and skeletal muscle constructs and their stimulation systems. By locating failures between excitation and force, researchers can interpret functional outcomes more precisely than by measuring electrical activity alone.