LEARNING OBJECTIVES
At the end of the session, the students should be able to:
• Describe Excitation-Contraction Coupling.
• Discuss the steps involved in spread of Action Potential in Skeletal
Muscle.
• Explain the Role of T-Tubules in Excitation-Contraction Coupling.
• Discuss Myasthenia Gravis.
Review of previous lecture
Excitation -Contraction Coupling
•Sequence of events by which transmission of an AP along the sarcolemma leads to sliding of the myofilaments
•Mechanism where an action potential causes muscle fiber contraction
Part of a skeletal muscle fiber (cell)
Events in Generation of an Action Potential
Release of Calcium From Sarcoplasmic Reticulum
•Dihydropyridine receptors
•Ryanodine receptors
•Calsequestrin
Summary of Excitation-Contraction Coupling
1End Plate Potential
2Muscle action potential depolarizes the T-tubule
3T-tubule depolarization activates the DHPR
4DHPR opens Ryanodine receptors
5Loads of Calcium is released from Sarcoplasmic Reticulum
6Calcium saturates Troponin C
7Tropomyosin is moved away from active sites
8Disinhibits Actin -myosin interaction
9Actin -myosin cycles the cross bridge
10Calcium reuptake by sarcoplasmic reticulum re-uptake shuts off contraction
Myasthenia Gravis
•Occurance: 1 in every 20,000 persons,
•Symptoms: Muscle weakness
•Pathophysiology: Auto-immune disorder . Antibodies that attack the acetylcholine receptors
•Antibodies block or destroy their own acetylcholine receptors at the postsynaptic neuromuscular junction.
•This leads to inability of the neuromuscular junctions to transmit enough signals from the nerve fibers to the muscle fibers.
•If the disease is intense enough, the patient may die of respiratory failure as a result of severe weakness of the respiratory muscles.
•Neostigmineor some other anticholinesterase drug, which allows larger than normal amounts of acetylcholine to accumulate in the synaptic space.
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