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.

Neurotransmitters, such as acetylcholine, are chemical signals that transmit action potentials from one neuron to another. This process occurs at the synapse, where a neurotransmitter is released from the presynaptic neuron. This neurotransmitter travels across the synaptic cleft and binds to a receptor on the postsynaptic neuron. Statement I is thus false.

The rate of propagation of a nerve signal is limited by the synapse because neurotransmitters must diffuse across the gap; statement II is true.

Calcium ions are very important in the release of neurotransmitters. Voltage-gated calcium channels are located on the axon of the presynaptic neuron. When an action potential reaches the synapse, calcium ions are allowed to enter into the presynaptic neuron. This influx of calcium ions interacts with vesicles containing neurotransmitters and causes them to release their contents into the synaptic cleft. Statement III is false because calcium ion channels are located on the membrane of presynaptic neuron, not postsynaptic neuron.

The SNARE proteins are responsible for allowing vesicles filled with neurotransmitter to fuse with the cell membrane at the synaptic cleft, resulting in exocytosis. Without these proteins, the neurotransmitter cannot propagate the signal to any other cells.

Neurotransmitter synthesis occurs via translation or synthesis in the smooth endoplasmic reticulum, depending on the identity of teh molecule. Resting potential is determined by the sodium-potassium pump, and action potential propagation relies heavily on voltage-gated sodium channels and myelin.

All of the choices could potentially be neurotransmitters.

Peptide neurotransmitters are proteins. An example of a peptide neurotransmitter is somatostatin. Nitric oxide is the most well-known gaseous neurotransmitter. Monoamines are molecules that contain an amine group connected to an aromatic ring. These molecules are derived from aromatic amino acids. Dopamine, norepinephrine, and epinephrine are very well-known monoamine neurotransmitters.  

Receptors on postsynaptic neurons are connected to ion channels. When the neurotransmitter binds to the receptor, the channel opens, making that neuron more or less likely to have an action potential depending upon which type of ion the channel allows to enter or exit the neuron. The result is either an excitatory postsynaptic potential (EPSP) or an inhibitory postsynaptic potential (IPSP).