Cross bridge cycling; Excitation-Contraction Coupling Flashcards
What factor causes myosin to detach from actin?
ATP binding to myosin crossbridge is required for actin to detach from myosin head, and allowing myosin to assumes its original conformation.
What causes the muscle cell to be excited?
Ca2+ ion binding to troponin
What happens when Ca2+ binds to troponin?
What causes power stroke?
Ca2+ binds to troponin will physically pull troponin-trypomyosin from myosin binding site on actin.
Powerstroke is refer to the bending of myosin head, which pulls actin inwards. Phosphate is used up during power stroke and ADP released after power stroke.
Ryanodine receptors
They are Ca2+ release channel on the lateral sac of sarcoplasmic reticulum
Where is Dihydropyridine (DHP) receptors located in skeletal muscles vs DHP receptors in smooth or cardiac muscles
DHP receptors in skeletal muscles are voltage gated receptors on T tubules that physically connect with ryanodine receptors, located on the membrane of the sarcoplasmic reticulum. They’re physical coupling allows the opening of calcium channels.
In smooth muscles, DHP receptors are located on the plasma membrane.
What event provides the energy for the power stroke of the cross bridge?
The splitting of ATP on the myosin head by myosin ATPase
What are the stages in contractile activity is ATP required ?
- ATP is required to bind to myosin to detach from actin.
- ATP needs to split by myosin ATPase to provide potential energy for the next power stroke crossbridge cycle
- ATP is required to transport Ca2_ back into the SR during relaxation, this depends on the energy derived from the breakdown of ATP
Since there is no troponin in smooth muscle cells, how do cross-bridge cycle occur?
In smooth muscle cells, increased cytosolic Ca2+ in the sarcoplasm causes a chain of events that activates myosin kinase activity, which phosphorylates “light-chain” proteins on myosin head.
phosphorylated myosin allows myosin cross-bridge binding with actin
What is the mechanism of Ca2+ action in smooth, skeletal and cardiac muscle cells?
Ca2+ induced a chemical change in myosin thick filament in smooth muscle cells. The chemical change brings about phosphorylation of myosin cross bridges so they can bind with actin
In skeletal and cardiac muscles, Ca2+ physically repositions troponin-tropomyosin complex to uncover actin-cross bridge binding sites.
Unlike in skeletal muscles, in which excitation induced ca2+ released from SR, increase in cytosolic calcium in smooth muscles comes from two sources….
Extracellular fluid predominately and some from SR. This is due to no T-tubules, or myofibrils in smooth muscles.
How is crossbridge activity different between smooth and skeletal muscle cells?
What is the function of dihydropyridine receptors in smooth muscles. How are they different from skeletal muscles?
Dihydropyridine receptors in skeletal muscles acts as receptors to open calcium channels. In smooth muscles, they open to allow the entry of ca2+ from outside of the cell. This entry of ca2+ triggers the release of ca2+ from the SR, thus influencing cross-bridge activity.
How do smooth muscle becomes excited to contract? what opens the Ca2+ channels in the plasma membrane?
What opens ca2+ channels in plasma membranes of smooth muscle cells depends if it is a multi unit or single unit muscle cell.
What does it mean when a cell (eg, smooth or heart muscle cells) are considered to be myogenic?
Myogenic means that the cells themselves are stimulated to contract by themselves rather than being stimulated by an outside event such as nerve stimulation.
How does contraction occur in smooth muscle cell?
Smooth muscle contraction is caused by the sliding of myosin and actin filaments over each other. The energy for this to happen is provided by the hydrolysis of ATP. Unlike cardiac contractile and skeletal muscle, smooth muscle does not contain the calcium binding protein troponin.
Which types of muscle cells are “self-excitable” ? (that it does not require nerves stimulation)
Single unit smooth muscle cells and auto rhythmic cells of the heart