Related Experiment Video
Updated: Aug 16, 2026
Generation of Local CA1 γ Oscillations by Tetanic Stimulation
Published on: August 14, 2015
Decrease in the size of tetanic responses produced by nitrendipine or by extracellular calcium ion removal without
Abstract:
The effects of removing extracellular Ca++ ions or of adding the organic calcium channel antagonist, nitrendipine, were tested on twitches and tetani (100 Hz for 2 sec) in frog toe muscles. Under conditions that did not reduce or that potentiated twitches, both procedures reduced the size of the tetanic responses. This depression was seen as an inability to maintain the maximum tetanic tension for more than 0.5 sec. Intracellular microelectrode recordings showed that the muscle fibers were depolarized (mean about 23 mV) during the stimulus train and the fiber only slowly repolarized after the train. The latter effect is the "late negative afterpotential" and it is produced by the accumulation of K+ ions in the t-tubules during the action potential train. Neither the depolarization nor the late negative afterpotentials were decreased in amplitude by nitrendipine. These results indicate that the voltage-sensitive, slow Ca++ channels are opened by the accumulation of K+ ions in the t-tubules during the tetanus and that the Ca++ ions entering via these channels are required to maintain the full strength of the tetanic contraction. It is suggested that this is a function of these Ca++ channels concentrated in the t-tubules of skeletal muscle fibers.
Insights
Removing calcium ions or using nitrendipine impairs frog muscle tetanic contractions. Calcium influx through voltage-sensitive channels in t-tubules is crucial for sustained muscle tension during tetanus.
Area of Science:
- Muscle Physiology
- Cellular Electrophysiology
Background:
- Skeletal muscle contraction relies on calcium ions.
- The role of calcium influx during sustained contractions (tetanus) is not fully understood.
Purpose of the Study:
- To investigate the role of extracellular calcium and specific calcium channels in maintaining tetanic muscle tension.
- To elucidate the mechanism of calcium ion involvement in frog skeletal muscle tetanus.
Main Methods:
- Frog toe muscles were subjected to tetanic stimulation (100 Hz for 2 sec).
- Extracellular calcium was removed, and the calcium channel antagonist nitrendipine was applied.
- Muscle tension and intracellular electrophysiology (microelectrode recordings) were measured.
Main Results:
- Both calcium removal and nitrendipine significantly reduced tetanic tension, impairing tension maintenance.
- Muscle fibers showed depolarization and a slow repolarization (late negative afterpotential) during tetanus.
- Nitrendipine did not affect the observed depolarization or late negative afterpotentials.
Conclusions:
- Voltage-sensitive calcium channels, likely in the t-tubules, are activated by potassium accumulation during tetanus.
- Calcium influx through these channels is essential for maintaining maximal tetanic muscle force.
- These findings highlight a specific role for t-tubule calcium channels in skeletal muscle function.
More Related Videos
07:42Contractions of Human-iPSC-derived Cardiomyocyte Syncytia Measured with a Ca-sensitive Fluorescent Dye in Temperature-controlled 384-well Plates
Published on: October 18, 2018
07:55Isolating Myofibrils from Skeletal Muscle Biopsies and Determining Contractile Function with a Nano-Newton Resolution Force Transducer
Published on: May 7, 2020
Related Concept Videos
01:17Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action
Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...
01:28Depolarizing Blockers: Mechanism of Action
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 succinylcholine...
01:26Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin
The binding of dantrolene to the RYR1...
01:21Skeletal Muscle Relaxants: Adverse Effects
Unlike...
01:29Relaxation of Skeletal Muscles
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.
01:18Antihypertensive Drugs: Action of Calcium Channel Blockers