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De La Salle Medical and Health Sciences Institute

College of Rehabilitation Sciences


CRS 101 & 102

A.Generation of an action potential

3
2

1 5

Phases of Nerve Action Potential

1. Resting Membrane Potential (RMP)


o State of having positive charge outside and negative charge inside the cell.

(C) Kim Aldrin R. Tuzon, PTRP


De La Salle Medical and Health Sciences Institute
College of Rehabilitation Sciences
CRS 101 & 102

2. Depolarization
o Opening of voltage gated Na+ channel (fast channel)
o Sodium influx causes positivity to the charge of the cell

3. Repolarization
o Rapid closure of voltage gated Na+ channel (fast channel)
o Opening of voltage gated K+ channel (Slow channel)

4. Hyperpolarization
o Slow closure of voltage gated K+ channel (slow channel)
o Causes the charge of the cell to be MORE NEGATIVE

5. Goes back to RMP again


o Made possible by Sodium-Potassium Pump (Na-K ATPase Pump)
o 3 Na+ goes out of the cell
o 2 K+ goes inside the cell

(C) Kim Aldrin R. Tuzon, PTRP


De La Salle Medical and Health Sciences Institute
College of Rehabilitation Sciences
CRS 101 & 102

B. Transmission in the NMJ

Once the AP arrives at the presynaptic terminal… (Refer to the number on the picture above)

1. Voltage gated Ca channels in the presynaptic membrane open and Ca ions enter the
pre synaptic terminal

2. Release of NT Ach from synaptic vesicles

3. Synaptic Vesicles secrete Ach into Synaptic Cleft by exocytosis

4. Ach binds to Ligand-Gated Na channels on the post synaptic membrane

5. Ligand gated Na channels open and Na enter the post synaptic cell

a. AP is generated along the post synaptic membrane (continuation at


excitation-contraction coupling)

6. Ach unbinds from the ligand gated Na channels

7. Acetylcholinesterase is released into synaptic cleft

a. Acetylcholinesterase breaks down Ach into Acetic Acid & Choline

8. Re-uptake of choline into pre-synaptic membrane;

9. Ach synthesis from choline recycled from the synaptic cleft and acetic acid generated
from metabolism in the presynaptic cell

(C) Kim Aldrin R. Tuzon, PTRP


De La Salle Medical and Health Sciences Institute
College of Rehabilitation Sciences
CRS 101 & 102

C.Excitation-Contraction Coupling
From the marked statement at number 5a, here is the continuation of AP. (Again, please
the description of the numbers below)

4. Ligand gated Na channels open and Na enter the post synaptic cell

a. AP is generated along the post synaptic membrane

5. Action potential propagated along the sarcolemma of


the muscle fiber, travelling to the T-tubule then into the
interior of the muscle fiber.

At this point, AP arrives at the Sarcoplasmic Reticulum


causing Voltage gated Ca channels of the terminal
cisternae to open

6. Calcium goes out of the sarcoplasmic reticulum and


travels towards the sarcomere.

7. Calcium ions bind to Troponin C


- Tropomyosin (serves as the covering) exposes the
active binding site at G actin leading to formation of cross
bridge

(C) Kim Aldrin R. Tuzon, PTRP


De La Salle Medical and Health Sciences Institute
College of Rehabilitation Sciences
CRS 101 & 102

D.Cross Bridge Movement

1. Phosphates are released from the myosin heads


2. Myosin head tilts
3. Actin slides past the myosin myofilaments
4. ADP is released from myosin
5. ATP binds to myosin heads
6. Detachment of myosin heads
7. New molecule of ATP is cleaved to begin the next cycle

What 3 events happen in the muscle fiber during muscle relaxation?

- Calcium is being pumped back to the Sarcoplasmic reticulum through active transport
- Active sites from the Actin are covered
- Myosin heads are released (Cross-Bridge release)

(C) Kim Aldrin R. Tuzon, PTRP


De La Salle Medical and Health Sciences Institute
College of Rehabilitation Sciences
CRS 101 & 102

References:

Hall, J. E., & Guyton, A. C. (2016). Guyton and Hall textbook of medical physiology (13th ed.).
Philadelphia (PA): Elsevier.

Seeley, R. R., VanPutte, C. L., Regan, J., Russo, A., Stephens, T., & Tate, P. (2017). Seeley's anatomy
and physiology (11th ed.). New York, NY: McGraw-Hill.

(C) Kim Aldrin R. Tuzon, PTRP

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