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Phys Lect 12

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)
Created by: WeeG



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