Pepsinogen is the inactivated form of pepsin. Pepsinogen gets activated by an increase in  ions (acid), which is released by the parietal cells. Pepsin helps with protein digestion and is released from the chief cells in the stomach. 

The tissues in the stomach are also made up of primarily protein. If it was produced in the stomach as its active form, then pepsin could also digest the stomach as well.

When at rest, the neuron initially has a negative membrane potential. At the beginning of an action potential, voltage-gated sodium channels open, allowing sodium ions to enter the cell. This causes the cell to become positively charged compared to the outside of the cell. This process is called depolarization.

After depolarization occurs, the sodium channels close, initiating the absolute refractory period. Voltage-gated potassium channels then open and potassium ions exit the cell. This results in hyperpolarization and the relative refractory period. The potassium channels then close and the sodium-potassium pump returns the cell to its resting potential by removing sodium and collecting potassium.

An action potential across a cell membrane has five phases:

1. The resting membrane potential is a negative membrane potential established by the sodium-potassium pump and maintained by potassium leak channels.

2. Depolarization involves opening of voltage-gated sodium channels and results in a rapid influx of positively-charged sodium ions into the cell, creating a positive membrane potential.

3. Overshoot occurs during the maximal value (peak) of the action potential.

4. Hyperpolarization occurs when sodium channels close and potassium channels open, allowing potassium to leak out the cell, and establishing a negative membrane potential below the resting potential.

5. Repolarization occurs when voltage-gated potassium channels eventually close and the membrane potential returns to the resting value via action of the sodium-potassium pump.

Potentiation refers to the phenomenon when nerves become more effective at transmitting signals due to extensive use of the same pathway.

Once an action potential has been created, the membrane has a period of time during which it cannot be stimulated to create another action potential. The absolute refractory period occurs when the voltage-gated sodium channels initially close. The first gating mechanism of these channels cannot be overcome by an electrical stimulus, and the sodium channels will remain closed even if a large electrical stimulus is present. During this period, even a very large stimulus cannot result in neural depolarization.

Following this, the secondary gating mechanism for the channel becomes active. This mechanism is sensitive to electrical stimuli, but keeps the channels closed when the neuron is at rest. The relative refractory period results when sodium channels are capable of opening, but the cell is hyperpolarized, making it very difficult to initiate a stimulus that reaches the action potential threshold.

The voltage-gated  channels along the axonal plasma membrane open and close in response to changes in voltage, and may exist in three distinct states: deactivated, activated, and inactivated. While the axon is at rest, these channels are said to be deactivated; they are impermeable to sodium ions since their activation gates are closed. Once the neuron gets depolarized to the threshold of the voltage-gated sodium channels, the activation gates open, allowing the influx of sodium down its concentration gradient into the cell. During this time the channels are in their activated state. At the peak of the action potential the activation gates are still open, but the inactivation gates close, stopping the flow of sodium through the channels. The channels are in the inactivated state due to the cell becoming depolarized. Once the membrane potential drops back down towards resting, the inactivation gates open, and the activation gates close, thereby deactivating the channels again, until another action potential depolarizes the membrane.

The neuron has a resting potential. In its resting state, the neuron has a resting potential with a slightly negative interior compared to the exterior. Sodium ions  enter the cell and alter the membrane potential. Through voltage-gated channels,  enters and makes the interior less negative therefore decreasing the membrane potential difference, which is known as depolarization. The membrane potential depolarizes all the way up to the threshold level. After enough  enters, the threshold membrane potential is reached. This opens more  channels. An action potential is fired, which means that the depolarization spreads down the neuron's axon. This travels down the entire axon, eventually reaching the dendrite and signaling to other neurons.

To support the general function of the nervous system, neurons must communicate within the cell (intracellular signaling) and between other cells (intercellular signaling). In order to achieve long distance and rapid communication, neurons have special abilities for sending electrical signals (action potentials) along axons. This mechanism is called conduction, and it is how the neuron's cell body communicates with its own terminals via the axon. Communication between neurons is achieved at synapses by the process of neurotransmission. 

At resting potential, the cell membrane is about 25 times more permeable to potassium ions than it is to sodium ions. During an action potential, the membrane becomes much more permeable to sodium ions than potassium ions, causing the membrane potential to become more positive, as sodium flows down its concentration gradient into the cell. Note that this concentration gradient is largely set up by the action of the sodium-potassium ATPase, which pumps three sodium ions out of the cell in exchange for two potassium ions into the cell. 

A synapse is a specialized junction between cells. It is involved in the integration and converging of signals between neurons. At a synaptic junction, the membranes of the pre- and post- synaptic neurons are separated by a gap called a synaptic cleft, which is the site of neurotransmitter release.