Sodium ions are positively charged (Na⁺) and enter the neuron starting at the axon hillock, which is where the axon and cell body come together. An influx of positively charged ions will cause the charge of the cell to increase.

When a neuron reaches threshold, it 'fires' an action potential down the axon using charge gradient to drive the propagation towards the axon terminal, where neurotransmitters will be released to relay the signal to the next cell.

Potassium ions are also positively charged (K⁺), but follow a gradient that promotes efflux over influx due to the equilibrium established by the sodium-potassium pump. As such, potassium flows out of a cells following depolarization, and actually results in the hyperpolarization observed immediately following an action potential.

It is the influx of calcium ions into the axon terminal that causes vesicles to fuse with the cell membrane, releasing the neurotransmitters held within the vesicles into the synapse.

Potassium ion (K⁺) influx happens during the refractory period, when the neuron returns to its membrane potential via action of the sodium-potassium pump. Potassium influx requires active transport. Sodium ion (Na⁺) influx is most closely linked with action potential propagation down the axon. It eventually triggers the calcium influx, but is not directly linked to vesicle fusion and neurotransmitter release.

Chloride (Cl^-) influx occurs when the neuron receives inhibitory signals, causing the cell to be hyperpolarized and not fire an action potential.

The refractory period is caused by two processes: the secondary gate closing the voltage-gated sodium channel to prevent sodium influx and the hyperpolarization of the neuron caused by potassium ion efflux.

The period of potassium efflux is closely linked to action by the sodium-potassium pump, which is responsible for importing potassium and ejecting sodium from the cell. During the refractory period, then, sodium is exiting the cell and potassium is entering. The cell is also It also removing the calcium ions that entered the axon terminal, inducing the neurotransmitter release, to prepare for further neurotransmitter release. This prepares it to fire another action potential once the refractory period is over.

The influx of sodium ions is linked to the propagation of action potentials, and would not occur during the refractory period due to the secondary gate on the voltage-gated sodium channel.

The Corpus callosum resides beneath the cortex in the brain and bridges the gap between the left and right cerebral hemispheres. It is involved in the transfer of information from these hemispheres, helping to integrate and coordinate bilateral responses.

The cerebrum is located in the cortex and is involved in higher brain function, such as thought and processing. The hypothalamus is involved in survival processes, such as the instinct to eat, drink, or reproduce. The cerebellum coordinates balance and fine-tuned movement. Purkinje cells are found in the cerebellum; Purkinje fibers are found in the heart.

Neuron function is highly dependent on ion concentrations. Sodium is required for depolarization, potassium for hyperpolarization and repolarization, and calcium is responsible for initiating neurotransmitter release. Vesicles of neurotransmitter are stored in the terminal end of the axon, opposite from the end with the axon hillock and cell body. When voltage-gated calcium channels open, the binding of calcium to these vesicles causes them to exocytose the neurotransmitter.

Myelin is the fatty substance that wraps around axons to create nodes of Ranvier. These nodes allow the depolarization signal to jump along the axon, rather than traveling fluidly. This method, known as saltatory conduction, allows the action potential to travel faster. Degeneration of myelin is associated with numerous neurological disorders.

It is true that the axon of one neuron transmits information to the dendrite(s) of another, but this contact is not direct. Neurons are separated by synapses, which are small gaps that neurotransmitters must cross in order to move from their original location to a new dendrite. The two neurons do not physically touch.

Depolarization results from the opening of voltage-gated sodium channels during the initiation of an action potential. Sodium has an electrochemical gradient that causes it to enter the cell when the channels open, resulting in a net flow of positive ions into the cell that increases the membrane potential. This increase is known as depolarization.

Potassium follows a gradient opposite to sodium. When voltage-gated potassium channels open, ions flow out of the cell and cause hyperpolarization.

Neurotransmitters bind to receptors on the dendrites, which causes an electrical signal to be sent to the cell body. The cell body then transfers this signal to the axon hillock before an action potential is sent down the axon. The axon terminates at the synaptic cleft, where it releases neurotransmitters to the dendrites of the next neuron.

Neurons can be unipolar, bipolar, or multipolar, depending on how many projections are coming off of the cell body. Bipolar neurons are found in the retina and inner ear, and have a single dendritic extension as well as a single axonal extension. Most neurons are multipolar; they have numerous dendrites and a single axon.

During the initial phase of an action potential, voltage-gated sodium channels open and allow sodium ions to enter the cell. This causes the membrane potential to rise to a positive value, resulting in depolarization.

Next, voltage-gated potassium channels open and potassium ions rush out of the cell. This reduces the membrane potential, resulting in repolarization as the potential becomes negative.

As more and more potassium exits the cell, the membrane potential declines below the resting potential, resulting in the hyperpolarized state. The sodium-potassium pump then functions to import potassium ions and export sodium ions to reestablish the resting membrane potential.

The relative refractory period is a time frame near the end of an action potential where another action potential can be generated only if a larger than normal stimulus is encountered by the neural cell. The relative refractory period takes place during the hyperpolarization of the cell. Since the membrane potential during hyperpolarization is more negative than the resting potential, it requires a much larger stimulus in order to reach threshold.