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1. AcH is released at
the neuromuscular junction.
2. End plate potential
occurs and migrates down the sarcolemma, through the T-tubules.
3. When it arrives at
the tip of the transverse tubular system, it will cause an inactive
enzyme to become an active enzyme.
As a result of that enzyme becoming active, a chemical product will be
hydrolyzed (split). It will split into two products.
One of those products will become a chemical SECOND MESSENGER.
That chemical second messenger will traverse the distance
between the t-tubule and the terminal cisternae, and
will bind to receptors that are located on the
terminal cisternae.
If enough of the receptors are activated, it will create a voltage
change in the membrane of the Sarcoplasmic reticulum.
4. When that voltage
change occurs, calcium gates will open on the sarcoplasmic reticulum.
5.
Since the concentration is greater in the Sarcoplasmic
reticulum than in the sarcoplasm, calcium will want to move down its
concentration gradient into the sarcoplasm until a threshold level of
calcium is reached in the sarcoplasm.
6. Calcium will bind
to troponin.
7. Troponin will
cause a conformational change of tropomyosin, allowing for interaction
between the actin and globular heads of the myosin filament.
8. Binding: The
myosin globular head will bind to the actin active site.
9. Bending: ATP
located on the myosin head is hydrolyzed (broken down) to ADP by
myosin ATPase. The energy released allows the Myosin molecule to
bend, moving the actin a slightly.
10. Breaking: ATP
reforms on the myosin head, allowing the myosin head to detach from
actin.
11. Bouncing: The
myosin head "bounces" to then next binding site, and the process of
binding, brending, breaking and bouncing continues. |
