Thursday, March 28, 2024

Application Question 13 -Black Widow Spider Latrotoxin

 
Application Question 13

    Due Mar 10 by 11:59pm Points 10 Submitting a text entry box Available until Mar 26 at 1pm

This assignment was locked Mar 26 at 1pm.

Look back over the responses from your classmates in the preceding discussion.  If you are satisfied with your original response to this question, simply copy and paste that response here!  If you wish to edit your original response based on what you saw in the discussion, make those changes before submitting.

Black Widow SpiderLatrotoxin is a compound produced by spiders in the genus Latrodectus (such as black widow spiders). Latrotoxin creates tiny holes in cell membranes at axon terminals that allow small hydrophilic particles to pass through the membrane.  Consider the above information and what we have learned thus far about activities in the neuromuscular junction.

What impacts would latrotoxin have on your muscles?

Discuss ACh, sodium, and calcium in your explanation.

Mostly Complete (10 pts): Muscles will be overstimulated/constantly contracting when exposed to venom.  Note that calcium would get into the axon terminal through the tiny holes and trace chain of events after that, including ACh and sodium.  View this video if you wish to review the steps that occur after calcium entry. Focus especially on the specific locations of ACh, calcium, and sodium and the order of the steps.

Partially Complete (6 pts): Answer is partially on track but incorrectly identifies the roles of either ACh, sodium, or calcium.

      Base on my understanding the sodium ions play a important role in muscle cell depolarization. Calcium ions are essential for muscle contraction. During normal muscle contraction, sodium channels open, allowing sodium ions to flow into the muscle cell.
           (1)   Latrotoxin effects affect cell membrane which sodium and calcium currents depolarize the membrane that allow influx of sodium and calcium ions .Binding to neuronal receptors disrupt normal neuromuscular junction function.

           (2)  Sodium ions play a critical role in muscle cell depolarization, when increase sodium ions into muscle cells triggers the release of calcium ions.

           (3)   Increase calcium ion [Ca2+] ion resulting in increase release ACH.  

           (4)   Excessive release of acetylcholine (ACH) at the neuromuscular junction,   resulting in increase muscle contraction of skeletal muscle and cardiac muscle.   Latroxin caused prolonged muscle contractions, spasms , muscle pain or  muscle damage.

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