Essay on Multiple Sclerosis and Action Potentials

Essay on Multiple Sclerosis and Action Potentials

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1. (10)
b. Explain why in multiple sclerosis the action potentials take longer to reach their muscle and neurological targets or do not reach them at all, resulting in muscle spasms and weakness in one or more limbs, bladder dysfunction, local sensory losses, visual disturbances and other neurological deficits.
c. Explain the speed of action potential in the normal person. Be sure to provide documentation using any example from the literature (provide the pdf-version of the article) and summary that supports your conclusion.

i. A neuron propagates action potential along its axon and then transmits this signal across a synapse by releasing neurotransmitters. Neurotransmitter triggers a reaction between another neuron or effector cell, which in turn stimulate or inhibit the receiving cell.
ii. An action potential is caused by the stimulus received by the dendrites of nerve cells. This stimulus causes the sodium channels to open. Opening of these channels causes the interior potential to go from -70 mV up to -55 mV. This allows for the cell to reach its action potential. When this potential is reached voltage gated sodium channels open and drive the potential inside the cell membrane to increase to around 30 mV. This is called depolarization. This action potential is conducted along the length of the fiber and causes the next adjacent space to open voltage-gated sodium ion channels to open. Once depolarized the sodium channels close and the potassium channels open, which allow for the membrane to repolarize to around -90 MV in a process called hyperpolarization. Hyperpolarization prevents the neuron from receiving another stimulus. After hyperpolarization the membrane goes back to its resting potential of -70 mV.
iii. Mye...

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2. Different species of dinoflagellates have different polyketide synthases, these synthases allow for the biosynthesis of saxitoxins.

d. What is its toxic dose? Is this an oral or iv dose?
i. The oral dose in humans that can result in human death is 1 to 4 mg. Unfortunately no further information can be found on this matter. However information of the LD50 for mice is available the oral and iv dosages are 3–10 μg/kg and 3400 ng/kg respectively.
e. If saxtoxin is such a powerful toxin in people who eat contaminated shellfish, why does the toxin not poison/kill the host shellfish?
i. The host/shellfish must have adopted a sodium ion channel that saxitoxins cannot bind to. For example some puffer fish have undergone a mutation that changes the amino acid sequence that makes its sodium channel insensitive to the toxin.
f. Sources:

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