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Phys Lect 12
Question | Answer |
---|---|
How are APs initiated in Skeletal muscle? | From an EPP with a large enough amplitude. |
Function of transverse T-tubules | Allow the spread of electrical excitation to the muscle interior from the Motor End Plate. |
Structure of transverse T-tubules | Invaginations of the muscle fiber membrane into the interior of the muscle cell. Each tubule is closely associated with a sarcoplasmic reticulum. **Also called Sarcolemma |
Location of transverse T-tubules in skeletal and cardiac muscle? | Skeletal: At the junction of A & I bands (Forms triads) Cardiac: down the Z-line (forms Dyads) |
Where is Ca2+ stored in muscle cells? | Sarcoplasmic reticulum |
Ryanodine Receptors (RyRs) or "Foot Proteins" | Large Ca2+ release channels in the SR. **Found directly between the T-tuble and SR. |
Dihydropyridine Receptor (DHPR) | Voltage-gated Ca2+ channels located in the T-tubule on top of the RyRs. |
Excitation-Contraction coupling of DHPR:RyRs in skeletal muscle? | 2:1. 4 DHPRs are found around one RyRs. However, this is only the case for every other RyRs, therefore 2:1 is the ratio instead of 4:1 |
How are RyRs opened in skeletal muscle to allow the Ca2+ out of the SR for a muscle contraction? | The DHPR and RyR are coupled. DHPR opens once depolarized by the AP traveling down the T-tubule. This causes the RyRs to open. |
Excitation-Contraction coupling: Is Ca2+ influx into the skeletal muscle cells through DHPR required for opening the RyRs? | NO |
How do the UNpaired RyRs open? (those not associated with DHPR) | they are activated by the Ca2+ released from the RyRs coupled with DHPRs |
Excitation-Contraction coupling of DHPR:RyRs in cardiac muscle? | 1DHPR:4RyRs. **Due to a low ratio, there is a Ca2+ induced Ca2+ release from the RyRs |
Excitation-Contraction coupling: Is Ca2+ influx into the cardiac muscle cells through DHPR required for opening the RyRs? | YES, due to the low number to DHPR to RyRs. |
What is the function of releaing Ca2+ from the SR? | Ca2+ binds to Troponin C and causes tropomyosin to shift, allowing myosin head to bind to actin. **W/o Ca2+: no crossbridges form, thus no contraction. |
Function of the High Affinity Ca2+ binding site on the RyRs | ACTIVATES the RyRs channel to open and release Ca2+ from the SR. **Ca2+ binds here at LOW cellular Ca2+ concentrations. |
Function of the Low Affinity Ca2+ binding site on the RyRs | INHIBITS the RyRs channel, causing it to close and STOPS the release of Ca2+ from the SR. **Ca2+ binds here at HIGH cellular Ca2+ concentrations. |
What terminates muscle contraction? | Removal of Ca2+ from the cytosol so no more can bind to Troponin C. |
3 mechanisms for removing Ca2+ from the cytosol of a muscle cell | 1.SERCA Pump back into SR (Primary mechanism). 2.Ca-ATPase pumps Ca out of cell. 3.Na-Ca antiporter (exchanges a Ca2+ for a Na+). **1 & 2 require ATP |
Malignant Hyperthermia | Genetic Mutation to the I (inhibitory) site of RyRs. Have an even lower affinity and in the presence of anesthetics (Halothane), the RyRs will not close |
Symptoms of Malignant Hyperthermia | 1.Rigor contractions (Constant Ca2+ supply). 2.Hyperthermia (High ATP use to pump Ca2+ back into SR). 3.High CO2 production (potential acidosis) |
Treatment for Malignant Hyperthermia interacting with Halothane? | RyRs inhibitors (sodium dantrolene) |