cross bridge cycle

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15 Terms

1
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<p>step 1</p>

step 1

an action potential arrives at the axon terminal of the motor neuron

2
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<p>step 2</p>

step 2

the calcium channels open, allowing calcium from the extracellular fluid to enter the synaptic terminal

3
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<p>step 3</p>

step 3

the vesicles within the synaptic terminal fuse with the pre-synaptic membrane, allowing acetylcholine to be released into the synaptic cleft

4
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<p>step 4</p>

step 4

the released acetylcholine attaches to the acetylcholine receptors on the motor end plate

5
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<p>step 5</p>

step 5

sodium from the extracellular fluid can enter the sarcolemma (i.e. depolarization)

6
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<p>step 6</p>

step 6

the action potential continues traveling through the transverse tubule

7
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<p>step 7</p>

step 7

the action potential’s travel triggers the release of calcium from the sarcoplasmic reticulum into the sarcoplasm

8
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<p>step 8</p>

step 8

calcium binds to troponin; tropomyosin shifts, exposing actin’s active site

9
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<p>step 9</p>

step 9

ATP binds to myosin and is hydrolyzed, while ADP and phosphate remain. The myosin head is cocked in a high energy position. Myosin binds to actin’s active site, forming a cross-bridge

10
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<p>step 10</p>

step 10

the release of phosphate, followed by the release of ADP from the myosin head triggers a power stroke. This causes the myosin heads to pull actin towards the center of the sarcomere

11
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<p>step 11</p>

step 11

a new ATP molecule attaches to the myosin head, causing the cross bridge to detach from actin

12
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<p>step 12</p>

step 12

the myosin head hydrolyzes ATP into ADP and phosphate. Myosin returns to its cocked position

13
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<p>step 13</p>

step 13

calcium is actively pumped back into the sarcoplasmic reticulum, which requires the use of ATP to make this possible

14
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<p>step 14</p>

step 14

calcium detaches from the troponin; tropomyosin shifts, covering actin’s active sites-stopping the cross-bridge-cycling and allowing the muscle fiber to relax

15
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<p>step 15</p>

step 15

acetylcholine is broken down by acetylcholinesterase, terminating the signal at the neuromuscular junction, preventing further depolarization of the muscle fiber