Anatomy: Test 3

Steps of a nerve impulse:

1. Release of ACh:

   a. nerve impulse » synaptic end bulbs cause Voltage-Gated Ca2+ channels to open » Ca2+ enters synaptic end bulbs

   b. Ca2+ causes synaptic vesicles to do exocytosis with the motor neuron plasma membrane to release ACh into synaptic cleft

2. Activation of ACh receptors:

   a. 2 molecules of ACh bind to ACh receptor on Motor end plate to open ion channel allowing Na+ to follow across membrane (Sarcolemma)

3. Production of muscle action potential:

   a. influx of Na+ » Muscle Action Potential

   b. Muscle Action Potential flows along sarcolemma into T tubules

   c. Causing SR to release Ca2+ to allow muscle contraction

4. Termination of ACh activity:

   a. Any ACh left in synaptic cleft gets broken down via acetylcholinesterase (found on extracell. side of motor end plate membrane)

   b. Muscle action potential ceases, ACh stops being released

   c. Ca2+ moves from Sarcoplasm » SR and Ca2+ channels in SR close

Contraction Cycle steps:

1. ATP hydrolysis:

   a. myosin head w/ ATP binding site and ATPase (to break down ATP into ADP and phosphate)

   b. ADP and phosphate attached to myosin head to energize myosin head

2. Attachment of myosin to actin to form cross-bridges

   a. energized myosin head attaches to myosin-binding site on actin (cross-bridge) » release phosphate group

3. Power stroke:

   a. cross bridge forms » power stroke » ADP binding site opens » ADP releases

   b. cross bridge generates force to allow thin filament to slide over thick filament toward M line

4. Detachment of myosin from actin:

   a. cross bridge remains attached to actin until bound with new ATP

   b. when ATP binds to binding site on myosin head, myosin detaches from actin

Excitation-contraction coupling:

1. In T tubules there are voltage-gated Ca2+ channels

2. Action potential go down T tubule then VG Ca2+ channels feel change in voltage then they change shape

3. This causes Ca2+ release channels to open and release Ca2+ from SR into sarcoplasm around myosin and actin

4. Concentration of Ca2+ rises and then binds to troponin which causes a conformational change to cause tropomyosin to uncover myosin binding sites on actin; myosin can now bind to actin and form cross bridges for muscle contraction

5. The membrane of the SR also has Ca2+ ACTIVE TRANSPORT PUMPS that use ATP to move Ca2+ back into SR from the sarcoplasm

6. If muscle action potentials continue to propagate through T tubules, Ca2+ release channels stay open and Ca2+ flows faster into sarcoplasm faster than transport back into the SR via Ca2+ active pumps

7. When last muscle action potential propagates, Ca2+ release channels close, Ca2+ active pumps move Ca2+ back into SR (Ca2+ levels in sarcoplasm decrease)

   • Protein Calsequestrin (inside SR) allows much more binding of Ca2+ to increase Ca2+ storage of SR

8. Ca2+ sarcoplasm levels decrease, Ca2+ released from troponin, tropomyosin covers myosin binding site on actin, muscle relax