toxicsugar22
  • toxicsugar22
Explain how the effect of myasthenia gravis is more similar, in some respects, to curare poisoning than to saxitoxin poisoning. Would you expect a person with henia gravis to have action potentials that are normal in scale?
Biology
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chestercat
  • chestercat
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toxicsugar22
  • toxicsugar22
@maddi4611 @aryandecoolest @adrynicoleb @partyqueen @GracieBugg @greatlife44 @RamiroCruzo @Robert136 @amber12362 @cxrulli
toxicsugar22
  • toxicsugar22
@Robert136
anonymous
  • anonymous
i need help on this too

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RamiroCruzo
  • RamiroCruzo
First of all, Myasthenia Gravis is caused by circulating antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction, inhibiting the excitatory effects of the neurotransmitter acetylcholine on nicotinic receptors at neuromuscular junctions. Now, Curare Poisoning is by competitively and reversibly inhibiting the nicotinic acetylcholine receptor (nAChR), which is a subtype of acetylcholine receptor found at the neuromuscular junction. And, Saxitoxin Poisoning contains neurotoxin that acts as a selective sodium channel blocker, it acts on the voltage-gated sodium channels of neurons, preventing normal cellular function and leading to paralysis. So, now Myasthenia Gravis & Curare Poisoning are more similar as they in simple words block the receptors whereas Saxitoxin blocks Na Channels. For the later question, yes, as Myasthenia Gravis is totally independent of ion channels.
RamiroCruzo
  • RamiroCruzo
Is it okay @toxicsugar22
Rushwr
  • Rushwr
Did u get it @toxicsugar22
RamiroCruzo
  • RamiroCruzo
Are you there @toxicsugar22
Rushwr
  • Rushwr
Myasthenia gravis is caused by a defect in the transmission of nerve impulses to muscles. Normally when impulses travel down the nerve, the nerve endings release a neurotransmitter substance called acetylcholine. Acetylcholine travels from the neuromuscular junction and binds to acetylcholine receptors which are activated and generate a muscle contraction. In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular which prevents the muscle contraction from occurring. Curare poisoning causes voluntary muscle paralysis by blocking impulse transmission between nerves and skeletal muscle. It doesn't paralyze smooth muscle at all (the type of muscle found in the heart, or intestinal tract). Curare attaches to the neuromuscular junction, blocking the transmitting material "Acetylcholine", disrupting future action potentials and making it insensitive to the action of acetylcholine. Until curare disintegrates, the nerve cannot trigger the muscle to act and the muscle stays paralyzed. Saxitoxin inhibits the temporary permeability of Na+ ions by binding tightly to a receptor site on the outside surface of the membrane very close to the external orifice of the sodium channel. It is a blocking agent that reduces the number of conducting Na+ channels . This prevents sodium ions from passing through the membranes of nerve cells, thus interfering with the transmission of signals along the nerves. The resulting widespread blockade prevents impulse generation in peripheral nerves and skeletal muscles. Saxitoxin has a direct effect on skeletal muscle by blocking the muscle action potential without depolarizing cells. So we can say curare poisoning is more likely to be like myasthenia gravis. Because both affect the neurotransmission by affecting the action of acetylcholine.
anonymous
  • anonymous
Would you expect a person with myasthenia gravis to have action potentials that are normal in scale? --- can you guys explain more on this

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