Muscular Dysgenesis A case study nervous and muscular physiology You are a resea

Question

Muscular Dysgenesis A case study nervous and muscular physiology You are a research scientist interested in finding the cause of the cellular defect associated with the genetic disease Muscular dysgeny. You already know it is a lethal recessive, genetic disease of mice that is caused by a mutation in the mdg gene. Animals with this mutation die shortly after birth. You are interested in finding the exact defect associated with this mutation. You surgically remove a single motor unit from a normal mouse fetus and a dysgenic mouse fetus. You place the neuron/muscle fiber unit in an experimental chamber in order to study abnormalities.

You briefly apply acetylcholine (ACH) directly to the motor end plate and observe the results. After ACH is applied to the muscle fiber, there is an AP generated on the sarcolemma of both the normal and dysgenic muscle fibers. Which of the following is NOT PROVEN by the above result? a) ACH receptors are present in the membrane of the motor end plate b) ACH binds to receptors c) Sodium permeability of the end plate membrane is increased d) Acetylcholinesterase breaks down ACH.

Explanation / Answer

The most appropriate choice is option d, i.e. acetylcholinesterase breaks down ACH.

When Ach was applied, action potential was generated. Thus, (a.) Ach receptors must have been present (b.) to which the Ach was bound, causing (c.) an increase in sodium permeability of the end plate membrane, which resulted in the action potential. However, whether acetylcholinesterase acts upon and breaks Ach cannot be inferred from the given observation.

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