1. (10)b. Explain why, in multiple sclerosis, action potentials take longer to reach their muscular and neurological targets, or do not reach them at all, leading to muscle spasms and weakness in one or more limbs, a bladder dysfunction, local sensory losses, visual disturbances and other neurological deficits. .c. Explain the speed of the action potential in the normal person. Be sure to provide documentation using any examples from the literature (provide PDF version of the article) and an abstract that supports your conclusion.i. A neuron propagates the action potential along its axon and then transmits this signal across a synapse, releasing neurotransmitters. The neurotransmitter triggers a reaction between another neuron or effector cell, which in turn stimulates or inhibits the receptor cell.ii. An action potential is caused by the stimulus received by the dendrites of the nerve cells. This stimulus causes the sodium channels to open. Opening these channels increases the internal potential from -70 mV to -55 mV. This allows the cell to reach its action potential. When this potential is reached, voltage-gated sodium channels open and increase the potential inside the cell membrane to approximately 30 mV. This is called depolarization. This action potential is conducted along the fiber and causes the adjacent space to open following potential-gated sodium ion channels. Once depolarized, sodium channels close and potassium channels open, allowing the membrane to repolarize to approximately -90 MV in a process called hyperpolarization. Hyperpolarization prevents the neuron from receiving another stimulus. After hyperpolarization, the membrane returns to its resting potential of -70 mV.iii. Mye...... middle of paper ......xin.2. Different species of dinoflagellates have different polyketide synthases, these synthases allow the biosynthesis of saxitoxins.d. What is its toxic dose? Is this an oral or intravenous dose? The oral dose in humans that can cause death is 1 to 4 mg. Unfortunately, no further information can be found on this subject. However, LD50 information for mice is available, oral and intravenous doses are 3-10 μg/kg and 3400 ng/kg, respectively. If saxtoxin is such a potent toxin in people who eat contaminated shellfish, why doesn't the toxin poison/kill the host shellfish?i. The host/mollusc must have adopted a sodium ion channel to which saxitoxins cannot bind. For example, some pufferfish have undergone a mutation that changes the amino acid sequence that makes its sodium channel insensitive to the toxin. Sources: I