Excitation of Skeletal Muscle: Neuromuscular Transmission and Excitation-Contraction Coupling

With the exception of a small percentage, how many neuromuscular junctions does a typical skeletal muscle fiber have?

What is the term for the invaginated membrane of the muscle fiber at the junction with a single axon terminal?

When a nerve impulse reaches the neuromuscular junction, approximately how many vesicles of acetylcholine are released from the terminals into the synaptic space?

The entry of which ion into the presynaptic nerve terminal is the primary stimulus for the release of acetylcholine?

What is the approximate diameter of the acetylcholine-gated channel, which is large enough to allow important positive ions to pass through?

Why are negative ions, such as chloride, prevented from passing through the acetylcholine-gated channel?

The opening of acetylcholine-gated channels creates a local positive potential change inside the muscle fiber membrane called the end plate potential. What is the typical magnitude of this potential change?

The normal neuromuscular junction is said to have a high safety factor because the end plate potential created is how many times greater than what is required to stimulate the muscle fiber?

At what rate of stimulation of the nerve fiber might the number of acetylcholine vesicles diminish enough to cause fatigue of the neuromuscular junction?

What is the approximate number of acetylcholine molecules stored within a single synaptic vesicle at the nerve terminal?

What is the mechanism of action of curare, a drug that blocks neuromuscular transmission?

Myasthenia gravis is an autoimmune disease that causes muscle weakness due to the inability of neuromuscular junctions to transmit signals properly. What is the underlying cause?

How does an action potential spreading along the surface of a skeletal muscle fiber reach the deep interior of the fiber to cause contraction?

In the T tubule-sarcoplasmic reticulum system, what is the direct consequence of a voltage change sensed by the dihydropyridine (DHP) receptors?

What is the function of the protein calsequestrin inside the sarcoplasmic reticulum?

Full excitation of the T tubule and sarcoplasmic reticulum system causes the calcium ion concentration in the myofibrillar fluid to increase from a resting state of less than 10 to the power of -7 molar to what peak concentration?

What is the approximate duration of the calcium pulse in a typical skeletal muscle fiber?

Malignant hyperthermia is a hypermetabolic crisis triggered in susceptible individuals by certain anesthetics. What is the direct cause of the sustained muscle contractions seen in this condition?

What is the resting membrane potential in skeletal muscle fibers, according to the text?

Which drug is administered to treat malignant hyperthermia by antagonizing ryanodine receptors and inhibiting calcium ion release?

What is the space between the nerve terminal and the muscle fiber membrane, which is typically 20 to 30 nanometers wide, called?

What is the primary function of the numerous smaller folds of the muscle membrane called subneural clefts?

In the adult acetylcholine receptor complex, which protein subunit replaces the gamma protein found in the fetal version?

The fusion of acetylcholine vesicles with the terminal membrane increases by approximately 10,000-fold when the intracellular calcium ion concentration increases by what factor?

What is the duration of an action potential in skeletal muscle?

What is the velocity of conduction of an action potential in skeletal muscle fibers?

Which protein is responsible for forming coated pits that lead to the reformation of synaptic vesicles in the terminal nerve membrane?

Which drug is a powerful nerve gas poison that inactivates acetylcholinesterase for weeks?

The weakness of the end plate potential at point C in Figure 7-4, which is too weak to elicit an action potential, is caused by what?

What is the function of the sarcoplasmic reticulum's terminal cisternae?

What is the collective term for the processes involved in the action potential causing the release of calcium ions, which then leads to muscle contraction?

When opened by acetylcholine, a single acetylcholine-gated channel can transmit 15,000 to 30,000 sodium ions in what time frame?

How much more negative is the resting membrane potential in skeletal muscle fibers compared to neurons?

How do drugs like methacholine, carbachol, and nicotine stimulate the muscle fiber?

What is the total number of subunit proteins that make up the fetal acetylcholine receptor complex?

The sequence of acetylcholine formation and release occurs within what time period?

How do drugs like neostigmine and physostigmine stimulate the neuromuscular junction?

What is the peak calcium concentration in the myofibrillar fluid during full excitation, which is required to cause maximum muscle contraction?

In the neuromuscular junction, what happens to the choline after acetylcholine is split by acetylcholinesterase?

A patient with myasthenia gravis is administered neostigmine. How does this drug ameliorate the condition?

What is the role of the voltage-gated calcium channels located on the inside surface of the neural membrane at the neuromuscular junction?

How many times faster is the duration of an action potential in a large myelinated nerve compared to that in skeletal muscle?

What is the relative conduction velocity in skeletal muscle fibers compared to the large myelinated nerve fibers that excite them?

The recycling of vesicles in the nerve terminal begins with the formation of coated pits, which break away to form new vesicles in about how much time?

The action of drugs like methacholine, carbachol, and nicotine often persists for many minutes to several hours primarily because they are what?

What is the composition of the sarcoplasmic reticulum?

How many acetylcholine molecules must attach to the acetylcholine receptor to cause a conformational change that opens the channel?

Where are the acetylcholine-gated ion channels located on the muscle fiber membrane?

What is the primary reason that far more sodium ions flow through the acetylcholine-gated channels than any other positive ions?

A sudden increase in nerve membrane potential of more than how many millivolts is normally sufficient to initiate an action potential at the muscle fiber membrane?