Excitation Contraction Coupling

Excitation contraction coupling.
prepared for physiology seminar.
won best seminar award,

1. Excitation Contraction Coupling (EC Coupling) - Akshay Gill ( Roll no. 17) MBB S 2018

2. Objectives: What is EC coupling? The passage of the impulse The T tubule Mechanism of Calcium Release The contraction sequence Relaxation Differences in smooth muscles Differences in cardiac muscles Applied aspect

3. What is EC coupling? An action potential triggers the contraction of a muscle cell. Calcium ions can regulate whether or not contraction can occur. Thus, “the link reaction which is needed to link muscle excitation (the depolarisation of the action potential) to Ca ++ release from the sarcoplasmic reticulum is called excitation-contraction coupling”.

4. Excitation sequence Contraction sequence Ec coupling

5. The Passage of the Impulse After the conduction of the impulse through the axons to the post-synaptic membrane via the neuromuscular junction, there are conformational changes leading to flux of Na + ions inside the muscle fibre. Accumulation of Na + within the cell commence the depolarisation of the membrane, giving rise to the end plate potential that keeps rising towards an action potential threshold.

6. The action potential that is crossing neuromuscular junction

7. Transfer of impulse towards Motor end plate

8. The action potential spreads throughout the fibre and specially within the T tubules. Deep inside the muscle fibre

9. The T-tubule : The T tubules are tube-shaped invaginations of the sarcolemma that penetrate throughout the muscle fibre. The lumen of the T tubule is continuous with the ECF, and the membrane depolarisation during action potential occurs across the T-tubule membrane. On either side of the T-tubule are swellings of the sarcoplasmic reticulum (SR) called the lateral sacs or terminal cisterns.

10. T tubule structure :-

11. How does depolarisation in the T-tubule membrane open a Ca ++ channel in the SR membrane? Located in the T-tubule membrane, closely associated with the foot of the SR Ca ++ Channel, is the T-tubule voltage sensor, better known as , DHPR (dihydropyridine receptor). The impulse passes to the L tubules containing another receptor – the RyR or Ryanodine receptor .

12. The voltage sensor, changes conformation in response to the depolarisation of the action potential, and causes opening of the - RyR (Ryanodine receptor) . This conformational change is transmitted to the foot of the SR Ca ++ Channel causing it to open, and allowing Ca ++ release. Thus, Ca ++ ions are released and utilised during contraction of the muscle fibres.

13. The Contraction Sequence that follows : The Ca ++ that accumulates, is the reason for initiation and maintenance of the contraction of sarcomere. The free Ca ++ binds with the troponin C protein component of the thin actin filaments introducing the active calcium-troponin complex.

14. Binding of Ca ++ to the troponin C

15. There is conformational change in troponin C, which induces alternation in the conformation of the tropomyosin protein. Exposure of the myosin binding sites of the actin filament.

16. Myosin head binds to the sites on the actin filament. The release of ADP+iP are tightly coupled to the power stroke, thus resulting in shortening of sarcomere.

17. Relaxation SERCA pump (Sarco- Endoplasmic Reticulum Calcium ATPase pump ) is the enzyme responsible for relaxation . This enzyme pumps calcium back into the sarcoplasmic reticulum from the cytosol.

18. Summary:

19. Differences in Smooth Muscles: Calcium channel differences: Different channels releasing calcium from ECF (RyR still exists though), depends on the type of smooth muscles. Channels could be voltage-gated, ligand-gated, second messenger-gated or mechanically-gated.

20. Calcium entrance options: From gated channels, extracellularly From IP3 IP3 (inositol triphosphate) is a second messenger that opens RyR channel which releases calcium from SR. III. Calcium binds to calmodulin. IV. Activation of MLCK (Myosin-light-chain- kinase ), causes phosphorylation of the myosin head.

21. Differences in Cardiac Muscles: Cells are coupled as electrical syncytium due to high expression of gap junctions between the cells. Gap junctions consist of 2 connexons, each made of 6 connexins. T tubules are very well developed with moe diameter DIAD is present, i.e. With 1-tubule, there is only 1 cistern.

22. Applied: Malignant hyperthermia : It is due to the mutation in the RyR located in the L-tubules . Characterised by – - increased body temperature - increased muscular contractions and muscle rigidity - increased heart rate - high fever

23. Any Queries?