The relative refractory period is the moment directly after an action potential when the neuron can only be stimulated to fire another action potential if there is a larger than normal stimulus. During an action potential, voltage-gated sodium channels open. After the action potential, the channels are gated and cannot be re-stimulated. This period is the absolute refractory period. The secondary gating is released, making the sodium-channels functional again, but the neuron has not been fully restored to resting potential. Release of potassium through voltage-gated potassium channels leads to hyperpolarization until the sodium-potassium pump is able to restore ion balance. This restoration takes longer than the un-gating of sodium channels, creating a period when the cell is hyperpolarized, but the voltage-gated sodium channels are capable of stimulation. If a large enough stimulus overcomes the cell hyperpolarization and reaches threshold, and action potential can still occur. This period is the relative refractory period.

While sodium and potassium maintain important functions in the conduction of action potentials along the axon of the neuron, it is calcium that is responsible for the binding of vesicles containing neurotransmitters to the pre-synaptic membrane. A severe lack of calcium would inhibit the release of neurotransmitters into the synaptic cleft. When the action potential reaches the axon terminal, it stimulates the opening of voltage-gated calcium channels. The resulting influx of calcium binds to synaptic vesicles, initiating the process to release their neurotransmitter contents into the synaptic cleft.

For an action potential to occur, voltage-gated sodium channels must open to cause a sharp depolarization (increase) in the membrane potential. Pairing that information with knowledge that action potentials originate at the axon hillock, no other answer choice makes sense. It is only logical, then, that a high density of voltage-gated channels be present at the location where action potentials are first initiated.

Saltatory conduction is a process that propagates an action potential more quickly down the length of an axon in a "leapfrog" manner. This propagation occurs in the gaps between myelin on an axon, called nodes of Ranvier. Without myelin, these nodes would not exist, and the rate at which an action potential is transmitted would decrease. People suffering with multiple sclerosis (MS) have myelin degradation, and thus have decreased motor and other neurological processes.

Electrical synapses transmit signals faster than chemical synapses due to the physical connection of neural cells through gap junctions. Chemical synapses are slower due to the action potential needing to arrive in the terminal bud, causing calcium channels to open. This causes neurotransmitter vesicles to fuse to the presynaptic membrane, releasing neurotransmitters to diffuse across the synaptic cleft.

Electrical synapses can allow bi-directional transmission of signals, but chemical synapses cannot. Saltatory conduction involves action potential propagation along the axon via the nodes of Ranvier, and is not involved in the synapse.

During the docking and fusion of synaptic vesicles, the increased levels of calcium in the synaptic terminal will lead to calcium ions binding to synaptotagmin, which facilitates the binding of V- and T-snares to initiate fusion. None of the other answer choices make sense with respect to vesicle fusion at the presynaptic terminal.

Metabotropic receptors involve the reception of a neurotransmitter via a G-protein signaling cascade. Muscarinic receptors are an example of metabotropic receptors.

Ionotropic receptors involve the binding of a neurotransmitter directly to an ion channel, and the ion channel subsequently opening and allowing its respective ion into or out of a cell.

As a result, ionotropic receptors elicit effects more quickly, as they do not involve intermediate steps.

During normal impulse conduction, 3 Na+ ions move out of a neuron while 2 K+ ions move in. This results in a high concentration of Na+ outside the cell and low K+ outside the cell. TXX will disrupt the electrochemical gradient by blocking the Na+/K+ voltage-gated channel. A patient suffering from TXX intoxication usually dies from respiratory paralysis brought on by the disruption of neural conduction along nerve fibers and axons. The most appropriate response to the question is the disrupted conduction of nerve impulses.

Depolarization occurs as the Na+ ions rush into the neuron. During depolarization, 3 Na+ ions move in and 2 K+ ions move out of the cell via the Na+/K+ pump. Repolarization returns the cell potential to its resting value by rushing K+ ions out of the cell. Hyperpolarization further decreases the cell potential after repolarization.

The axons are myelinated by oligodendrocytes. This question calls on our knowledge of the nervous system outside of what is stated in the passage. We are looking for the most likely explanation for the increase in the frequency of the action potential. Myelinated nerves have the ability to increase the frequency of action potential conduction. Therefore, we can narrow the options down to either myelinated by Schwann cells or oligodendrocytes. The question then becomes: Which cells are responsible for the myelination? In both cases, glial cells are responsible for laying down the myelin sheath. In the central nervous system (CNS), these cells are called oligodendrocytes, while in the peripheral nervous system they are called Schwann cells. Since we are talking about nerves located in the CNS, the correct answer is oligodendrocytes.