In excitation-contraction coupling of skeletal muscle, which structural interaction between the transverse tubule voltage sensor and the sarcoplasmic reticulum Ca²⁺ release channel is responsible for Ca²⁺ release WITHOUT a requirement for extracellular Ca²⁺ influx?
- A T-tubule depolarization opens DHPR allowing Ca²⁺ influx which binds to RyR2 on the SR via Ca²⁺-induced Ca²⁺ release (CICR)
- B IP3 generated by PLC-β at the T-tubule membrane diffuses to open IP3R on the SR membrane
- C L-type Ca²⁺ channels (DHPR) in T-tubules undergo voltage-dependent conformational change that mechanically activates RyR1 on the SR membrane via physical protein-protein interaction ✓
- D Voltage-gated Na⁺ channels in the T-tubule trigger local Na⁺ influx that displaces Ca²⁺ from the SR lumen
Explanation
Skeletal muscle E-C coupling differs from cardiac muscle in that it is independent of extracellular Ca²⁺. DHPR (dihydropyridine receptor, Cav1.1 L-type Ca²⁺ channel) in the T-tubule membrane acts as a voltage sensor. Upon depolarization, DHPR undergoes a conformational change (voltage-induced structural shift) that is physically transmitted via direct protein–protein coupling ('tetradic' interaction) to RyR1 (ryanodine receptor type 1) on the adjacent SR membrane, causing it to open and release Ca²⁺ from the SR lumen. This is mechanical (conformational) coupling — no Ca²⁺ influx through DHPR is needed. In cardiac muscle, DHPR opens and the small Ca²⁺ influx triggers Ca²⁺-induced Ca²⁺ release (CICR) via RyR2.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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