General Neuron Physiology - Anatomy

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.

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 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.

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.

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.

Glutamate opens sodium channels in the plasma membrane of the receiving neuron, moving the action potential towards (depolarize) the sodium Nernst potential (81mV). GABA is an inhibitory neurotransmitter which opens chloride channels in the plasma membrane of the receiving neuron, making the neuron more difficult to excite (hyperpolarized).

The action potential of a neuron is generate at the axon hillock and is propagated down the axon and to the terminal branches where it will synapse with the dendrites of the next neuron.

Depolarization is when the neuron becomes more positive by gaining positively charged ions, specifically sodium ions. During depolarization the sodium ion channels open and sodium ions enter the neuron, reducing the membrane potential to roughly +35 mV.

In order to have an action potential, you must have a depolarization. Na channels must close before K channels open

Myelin helps to increase resistance along the axon, which helps to propagate the action potential along the axon.

The influx of positive sodium ions into the neuron is known as depolarization. This is the loss of negative charge that occurs when positive sodium passes through the neural membrane and enters the neuron.

The resting membrane potential is based on the difference in electrical charges of the ions that flow through the membrane. The membrane potential has a greater permeability to potassium when at rest which causes a shift in its potential. Thus, potassium has the strongest affect on the RMP and causes it to be closer to potassium's reversal potential. Side note: This potential is strongly held by the sodium potassium pump.

If an already positive membrane potential becomes more positive, it is becoming hyperpolarized because the electrical difference between the inside and outside of the cell is getting larger. On the other hand, a stimulus that moves the potential difference closer to 0 is depolarizing because it is decreasing the difference in electrical potential between the inside and outside of the cell.

Once an action potential has reached the end of the presynaptic neuron, voltage-gated calcium channels are stimulated, allowing calcium to enter the neuron. This influx of calcium stimulates the release of neurotransmitters into the synaptic cleft.

The neurotransmitters then bind to receptors on the surface of the postsynaptic neuron to generate small electrical stimuli. The sum of these stimuli must reach threshold in order for an action potential to be generated.

GABA and acetylcholine are two common neurotransmitters. GABA generally inhibits the postsynaptic neuron, while acetylcholine generally excites/stimulates the postsynaptic neuron.

Neurotransmitters will never enter the postsynaptic neuron. They will attach to receptors on the membrane of the postsynaptic neuron, release, and then be dealt with while in the synaptic cleft. In some instances, the neurotransmitter simply diffuses away from the synapse, but in most cases synaptic proteins help to recycle the molecules. Some enzymes will break the neurotransmitter into parts, which then reenter the presynaptic neuron and are reassembled. Acetylcholinesterase is a common example of this type of enzyme. Other neurons use membrane pumps to retrieve neurotransmitter from the synaptic cleft.

Acetylcholine activates muscarinic receptors in postganglioinic parasympathetic nervous tissue and nicotinic receptors in skeletal muscle fibers, and preganglionic sympathetic and parasympathetic nervous tissue.

Neurotransmitters are packaged in vesicles, traveling through the synaptic cleft (space between neurons) from the pre-synaptic membrane to the post-synaptic membrane, where they bind to their receptors and influence the post-synaptic membrane potential.