Answer:
The correct answer is ''loss of acetylcholine receptors in the end-plate membrane.''
Explanation:
Myasthenia gravis represents a human autoimmune disease. The neuromuscular junction abnormalities that occur in this disease are due to antibody-mediated processes. A reduction in the number of functional acetylcholine receptors on the postsynaptic membrane was established to contribute to the physiological abnormalities of myasthenia gravis. The reduction in receptors is due to immunological alterations directed against the acetylcholine receptor. Normally, when acetylcholine binds to its receptor, it opens allowing the rapid entry of cations, especially sodium. With this, the depolarization of the postsynaptic region of the muscle fiber occurs. Although acetylcholine is normally released in myasthenia gravis, it is not capable of causing an action potential in the muscle sufficient to initiate or weaken contraction. In patients with myasthenia gravis, failure to activate muscles is responsible for myasthenic fatigue. Most patients have elevated serum titers of antireceptor antibodies, which in turn accelerate receptor degradation.
Answer: principle of neuroplasticity.
In the result of the brain damage, amir stopped moving the left side of his body and after rehabilitation <span>he partially regained its functions. Why? because of</span> neuroplasticity. The brain, especially in children, has the ability of being plastic, meaning that the brain activity
associated with a given function, can be transferred to a different
location. This process is achievable through rehabilitation.
Yes, A-T and C-G, or vice versa.
Answer:
Circulatory system
Explanation:
It flows through your blood and it can affect your veins,arteries,heart,ect
