MSK 20 - Muscle Physiology-I Flashcards
What type of ACh receptors in the NMJ?
nicotinic
What does the EPP depend upon? What occurs if the EPP does not reach threshold?
Magnitude of EPP depends upong the amount of Ach released (graded response)
If EPP does not reach threshold then it dissipates and no AP occurs
What is a T-tubule and what is its purpose?
Transverse tubules (T-tubules) are extensions of the sarcolemma that penetrate into the centre of skeletal and cardiac muscle cells. The contain large amounts of ion channels that allow action potentials to enter rapidly into the cell, to initiate muscle contraction.
Differentiate the L-type calcium channel from the ryanodyne receptor from the dihydropyridine receptor.
L-type calcium channel/dihydropyridine receptors are the same thing. They are voltage gated calcium channels they stay activaged for longer (L-type) than usual. They also take a long time to become activated. In skeletal muscle, their purpose is to sense a voltage change and undergo a conformational change that opens the ryanodyne receptor in the SR membrane. Very little to no Ca++ passes through the DHP receptors.
Describe how an EPP leads to an increase in cytosoloic [Ca2+] in skeletal muscle cells.
Once an EPP reaches threshold the V-gated Na+ channels at the edge of the motor end plate open up triggerin an AP wave across the sarcolemma that continues into the T-tubules. The L-type V-gated Ca++ channel then undergoes a conformational change that then opens the ryanodyne receptor on the SR. This releases Ca++ from the SR into the cytosol.
Why is the L-type sensor an important adaptation for skeletal muscle?
How does cytosolic {Ca++] decrease again during skeletal muscle relaxation?
The sarco/endoplasmic reticulum Ca++ ATPase or SERCA actively pumps Ca++ from the cytosol back into the SR.
What is calsequestrin and why is it important?
Calsequestrin is a Ca++ binding protein found within the SR. It serves to decrease the free [Ca++] in the SR assisting SERCA in pumping Ca++ into the SR against a concentration gradient.
How does an increase in cytosolic [Ca++] casuse muscle contraction?
Ca++ binds to tropinin-C (TnC) causing a conformational change that will move tropomyosin from the mysoin binding sites on actin. This will the allow crossbridge cycling to occur.
Decribe the concept of all or none contraction.
Describe the entire myosin crossbridge cycle
How controls the rate of crossbridge cycling? Can this be modifided in skeletal muscle?