The period of time immediately after an action potential passes will be characterized by an immediate reduction in membrane potential, followed by hyperpolarization. At this point in time, the sodium voltage-gated channels are inactivated, halting the overshoot and influx of sodium ions into the cell. These channels remain inactivated, in order to avoid having the voltage-gated sodium channels open again to trigger another action potential. This is considered the absolute refractory period. The voltage-gated potassium channels are slower to open than the voltage-gated sodium channels. By the time the sodium overshoot has peaked, the voltage-gated potassium channels are open, allowing an efflux of potassium out of the cell. The efflux is responsible for lowering the membrane potential and eventually causing hyperpolarization.

An electrical stimulus causes voltage-gated sodium channels in a neuron to open. Sodium then travels down its concentration gradient through the channels, into the cell. With the movement of sodium into the cell, the cell depolarizes (its membrane potential becomes more positive). The gradient that drives depolarization is established by the sodium-potassium pump, which causes two primary effects: the resting membrane potential is negative and there is a large concentration of sodium outside of the cell. When sodium channels open, sodium ions flow down both the electrical gradient formed by the negative membrane potential and the chemical gradient formed by ion concentrations.

During the generation of an action potential, the cell will undergo two refractory periods. The first is referred to as the absolute refractory period, during which no stimulus, regardless of size, will generate another action potential. This is followed by the relative refractory period, during which an action potential will be generated only if an abnormally large stimulus is encountered. During the relative refractory period, the cell is hyperpolarized due to the removal of potassium ions from the cell interior, which results in a more negative membrane potential than the cell would have at rest.

The resting potential of a cell is roughly –70mV. When the potential rises above this level, the cell is considered "depolarized." When the potential delves below this level, the cell is considered "hyperpolarized." If the cell is depolarized above –55mV, the threshold potential, then an action potential is triggered.

Hyperpolarization occurs because potassium channels are slow to open and close, and thus the cell polarizes itself beyond its usual membrane potential. After an action potential depolarizes a cell there is a build-up of positive charge in the cell interior. The late opening of potassium channels causes an abrupt rush of potassium out of the cell, propelled by its electrochemical gradient. This rush lowers the cell potential below its normal resting state, resulting in hyperpolarization. The cell then returns to its resting state via repolarization. Sodium is removed from the cell and potassium is reintroduced through action of the sodium-potassium pump.

Graded potentials reflect stimulus strength because they do not propagate via saltatory conduction (as action potentials do), and thus decrease in amplitude down the axon. All other answers listed are characteristics of action potentials.

Once the cell reaches threshold, an action potential is fired. Sodium, a positive ion, enters the cell, and causes the charge on the membrane to rise, or depolarize. After a certain point, sodium gates close. Potassium, another positive ion, then leaves the cell, and the charge on the membrane decreases. As the potassium ions exit, the membrane potential plunges even lower than the resting potential, causing it to become hyperpolarized. At this point, the sodium/potassium pump works to repolarize the cell to return to the resting membrane potential.

1. The cell reaches threshold

2. Sodium gates open, and sodium floods into the cell

3. The cell depolarizes

4. Sodium gates close

5. Potassium gates open and potassium leaves the cell

6. The cell hyperpolarizes

7. Potassium gates close

8. Na/K pump repolarizes the cell during refractory period

All muscle types (cardiac, skeletal, and smooth), require sodium to enter the cell to initiate an action potential. The action potential then travels down the axon, elicits neurotransmitters, activates calcium channels, and causes the muscle to contract. In order to initiate the action potential, sodium must enter the cell in large quantity. This depolarizes the cell above the action potential threshold. If the cell does not reach the action potential threshold, then there will be no action potential and no muscle contraction.

When sodium ions enter the neuron, the membrane begins to lose its negative charge and therefore become depolarized. Hyperpolarization, repolarization, and polarization all occur with the efflux of  potassium ions out of the neuron. Note that an action potential stimulates the influx of sodium ions. The sodium potassium pump uses ATP to drive the establishment of the resting membrane potential by pumping three sodium ions out of the cell in exchange for two potassium ions into the cell. Both of these ions are being pumped against their concentration gradients. Neurotransmitter release is stimulated by the influx of calcium ions.

First it is important to realize that there is a higher concentration of potassium ions inside of the cell and a higher concentration of sodium ions outside of the cell. When depolarization occurs, sodium ion channels open. With this information, we can get rid of any answer choices that do not mention sodium ions. Now we must see if sodium ions enter or exit the cell. Since there is a higher concentration of sodium ions outside of the cell, sodium ions will enter the cell by going down the concentration gradient. 

Neurotransmitters in the human body are under tight control. Many drugs, such as anti-depressants or drugs for ADHD, limit neurotransmitter responses. Antagonistic molecules will inhibit neurotransmitters and are used in many drugs. These molecules structurally interact with receptor proteins, either blocking the active site or binding allosterically to alter the binding site shape. Antagonists can be competitive or uncompetitive.

In contrast, agonists are molecules that structurally resemble the ligand for a certain receptor and can bind to the active site to trigger a response. Nicotine, for example, is an agonist to certain acetylcholine receptors and can trigger these receptors.