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So voltage of EPP is much more than required, because required is only 25 mV. It is called as SAFETY FACTOR.
Action potential
Independent of stimulus strength (all or none) Propagated, unchanged in magnitude
These channels have 5 sub-units: 2 alpha sub-units which protrude out on surface & 3 others are beta, gamma & delta. Ach synthesized in synaptic knob vesicle released recycled.
Mitochondria energy Ach formation from CoA & Choline synaptic knob. Impulse reaches agitation of vesicles Ach binds with receptors Ach esterase acetate & choline recycled.
MYASTHENIA GRAVIS:
A rare auto-immune disease. More common in females Voltage of EPP is very low (Miniature EPP) action potential is not followed. At rest normally, a few synaptic vesicles break to liberate Ach from synaptic vesicles small change in EPP (about 0.5 mV) called MEPP. Impulse fails to transmit through NMJ Severe muscle weakness & fatigue. Auto-antibodies are produced against Ach gated receptor channels & these receptors are destroyed irreversibly, though Ach is present
2. Plasmapharesis: it may sometimes be needed to remove the autoantibodies from the serum. 3. Glucocorticoids (steroids) may also be required to inhibit the immunity.
Evidence that Myasthenia Gravis is an autoimmune disease: 1. Auto antibodies detected in patients blood. 2. In many of these cases, thymus is enlarged & thymectomy is of benefit.
3. If mother is myasthenic, newborn shows features of myasthenia for few weeks because antibodies cross the placenta. But antibodies die in few weeks, due to limited life span. They will destroy few receptors, which will regenerate later.
EXPLANATION OF CASE
This young woman has classic myasthenia gravis. In the autoimmune form of the disease, antibodies are produced to ACh receptors on the motor end plates of skeletal muscle. Her symptoms of severe muscle weakness (eye muscles; arms and legs) are explainable by the presence of antibodies that block ACh receptors. Although ACh is released in normal amounts from the terminals of motoneurons, binding of ACh to its receptors on the motor end plates is impaired. Because ACh cannot bind, depolarization of the motor end plate (end plate potential, EPP) will not occur, and normal action potentials cannot be generated in the skeletal muscle. Muscle weakness and fatigability ensue.