Those Myofiloments : How They Move: The Basis of Muscle Contraction

1. Those Myofiloments: How They Move: The Basis of Muscle Contraction Plus: The Neuromuscular Junction: where it all happens: This IS Muscle Physiology!

2. WHAT IS THRESHOLD? • A little stimulus….a few gates open…some Na+ influx…. WE CALL THIS A LOCAL POTENTIAL . Occurs at the soma. NOT on the axon. • More stimuli needed to reach THRESHOLD which will open VOLTAGE-GATED gates. • These located on TRIGGER ZONE. • NOW lots of Na+ ion will influx AND we have AP! • Critical voltage for threshold is -55mV

3. Figure 11.4

4. The Case of the Shrinking Sarcomere • SEE THE I BAND DISAPPEAR during a contraction of the.. sarcomere? Yes. Which makes up myofibers. • Will the I band reappear? When? • What causes the I band to dissapear?

5. The Case of the Shrinking Sarcomere • SEE THE I BAND DISAPPEAR during a contraction of the.. sarcomere? Yes. Which makes up myofibers. • Will the I band reappear? When? • What causes the I band to dissapear?

6. What is ACTUALLY happening when a Sacromere Shrinks? • The thin filament ACTIN and the THICK filament MYOCIN form a CROSS-BRIDGE that cause a SLIDING motion. • This shortens the sacromere or closes that GAP or I band and causes a CONTRACTION. • Neither the ACTIN nor the Myocin filament actually shorten its the sacromere itself.

7. So …..HOW DO WE GET THE CROSS-BRIDGE BETWEEN ACTIN AND MYOSIN???

8. THE MYOFILAMENTS First we need to learn about the ultrastructure of the ACTIN filament and its Subunits……….

9. ACTIN’s Ultrastructure • Fibrous F-Actin- This is the double-stranded protein (looks like a beaded necklace). • Globular G-Actin- These are the subunits of F-actin- contain active sites for myocin heads • Topomyosin- This is the filament that blocks the myosin sites. • Troponin- Found on tropomyosin, this protein binds w/ Ca++ . When it does, the configuration of tropomyosin will change…..the sites for myosin on ACTIN will become EXPOSED.

11. ACTIN and MYOSIN MUST BIND TO FORM a CROSS-BRIDGE, BUT HOW??????

12. Figure 11.3a

13. OBSERVE THE UNCOVERED ACTIN SITES…MYOCIN CAN NOW BIND…

14. Classification of these Proteins? • Actin and Myosin ( CONTRACTILE PROTEINS..because they do the work of shortening the muscle fiber) • Tropomyosin and Troponin (Regulatory proteins- because they are like a switch that can be turned on and off.)

15. A Series of Events Must Occur Before Ca++ is Bound to Troponin: Let’s Begin • The control of the CONTRACTION is derived from the NERVOUS SYSTEM • The specialized intercellular connection between the nervous system and the muscle is known as the NEUROMUSCULAR JUNCTION

16. The Muscle Cell: A Specialized Cell: Called a myocyte, but better term is… Muscle Fiber.

19. Figure 11.5

20. Figure 11.6

21. The Neuron

22. STRUCTURE and FUNCTION NEURONS/ The Synaptic Cleft

24. MOTOR END PLATE • This is where the neuron and myofiber intercept. • Muscle contraction is possible because of neural impulse at the motor end plate. • It is the action potential that causes the release of Ca++ ions from the SR, • The Ca++ can then bind to Troponin and change the configuration of Tropomyocin. • ACTiN’s G binding sites are then exposed.

25. Ionic Basis of Resting Membrane Potential • Na+ concentrated outside of cell (ECF) • K+ concentrated inside cell (ICF)

26. The SR Stores Ca ions and Release them When There is an AP! Find the T-Tubules

27. What happens to Plasma Membrane of Neuron to Generate a AP? From RESTING STATE to DEPOLARIZATION: The stimuli from the environment are going to cause the sodium gates to OPEN and there will be in INFLUX of Na+ ions going into the cell. RESULT: The negative charge (-70) starts to become less negative, depending on how much Na+ ions go in that gate! This is the D E P O L A R I Z A T I O N

28. What is the MEMBRANE POTENTIAL? • We Will Be Using the Term • MEMBRANE POTENTIAL • This is the voltage difference between the interior and exterior of the plasma membrane . In this case it’s the sarcolemma.

29. Sending information (Cont.) Definition of AP: action potential is a tiny electrical current that is generated when the positive sodium ions rush inside the axon’s plasma membrane. What does This DO? the enormous increase of Na ions inside the axon’s plasma membrane. This causes the inside of cell to reverse its charge The inside of cell becomes positive & the outside becomes negative

31. Action Potentials • Called a spike • Characteristics of AP • follows an all-or-none law • voltage gates either open or don’t • nondecremental (do not get weaker with distance) • irreversible (once started goes to completion and can not be stopped)

32. Ionic Basis of Resting Membrane Potential • Na+ concentrated outside of cell (ECF) • K+ concentrated inside cell (ICF)

33. WHAT IS THRESHOLD? • A little stimulus….a few gates open…some Na+ influx…. WE CALL THIS A LOCAL POTENTIAL . Occurs at the soma. NOT on the axon. • More stimuli needed to reach THRESHOLD which will open VOLTAGE-GATED gates. • These located on TRIGGER ZONE. • NOW lots of Na+ ion will enter the cell AND we have AP! • Critical voltage for threshold is -55mV

34. INSIDE-0UT!!!GO!!!

36. Sodium-Potassium Pump: (Remember Me?)

37. Excitation (steps 1 and 2) • Nerve signal opens voltage-gated calcium channels. Calcium stimulates exocytosis of synaptic vesicles containing ACh = ACh release into synaptic cleft.

40. Excitation-Contraction Coupling

41. T-Tubules Get Excited • 1. Acetylcholine ,released by the synaptic terminal, binds to receptors on the sacrolemma. • 2. There is a resulting change in transmembrane potential which leads to an action potential that spreads along the T-tubules. • 3. This is the signal to the SR to release Ca++ ions into the sarcoplasm in and around sarcomeres. • 4. Ca++ binds to Troponin. ,producing configuration change thereby exposing Myosin binding sites.

42. The Role of ATP in Cross-Bridging • After sites on Actin have been exposed… • Repeated Cycles of cross-bridging occur as myocin heads pivot, detact and reattach. • EACH ATTACHMENT IS POWERED BY THE HYDROLYSIS OF ATP • ATP -- ADP + P (High energy phosphate is used for cocking the myosin head into position.)

44. Excitation-Contraction Coupling (steps 8 and 9) • Calcium released by SR binds to troponin • Troponin-tropomyosin complex changes shape and exposes active sites on actin

45. CONTRACTION • Myosin ATPase in myosin head hydrolyzes an ATP molecule, activating the head and “cocking” it in an extended position • It binds to actin active site forming a cross-bridge

46. Contraction • Power stroke = myosin head releasesADP and phosphate as it flexes pulling the thin filament past the thick • With the binding of more ATP, the myosin head extends to attach to a new active site • half of the heads are bound to a thin filament at one time preventing slippage • thin and thick filaments do not become shorter, just slide past each other (sliding filament theory)

49. Myoglobin • Myoglobin is oxygen carrier ( It is a pigment) • Synthesized in muscle • Higher affinity for oxygen than hemoglobin • One globin protein, rather than 4: therefore we say this protein has tertiary level structure as apposed to hemoglobin’s quartenary level structure. • It can STORE oxygen as well as carry it.

50. Creatine Phosphate • This a high energy molecule found in muscle cells • 4 to 6 time more abundant in muscle fibers than ATP!! • It CANNOT directly transfer a phosphate group to a reaction • INSTEAD, when ATP is sufficient an enzyme in mitochondrian, creatine phosphokinase promotes the synthesis of creatine phosphate. • As ATP gets degraded, creatine phosphate can donate its phosphate bonds to ADP creating NEW ATP