35.2 How Neurons Communicate

glial cells help maintain the environment.

The central nervous system contains glial cells.
The myelin sheath surrounds axons.
Astrocytes provide support to the brain.
The cells produce fluid in the brain.
Schwann cells and satellite cells are part of the peripheral nervous system.

By the end of this section, you will be able to discuss the basis of the resting membrane potential, explain the stages of an action potential, and describe long-term potentiation.

Humans use words and body language to communicate.
Just like a person in a committee, one neuron gets messages from multiple other neurons before making a decision to send the message to other neurons.

The nervous system must be able to send and receive signals.

The charge of the cell'smembrane can change in response to neurotransmitters released from other neurons and environmental stimuli.
The basis of the baseline or'resting' membrane charge is the first thing one needs to understand how neurons communicate.

The lipid bilayer is impermeable to charged particles.

The ion channels that span the membranes must be passed through to enter or exit the neuron.
The ion channels need to be activated in order for the ion to pass into or out of the cell.
The environment can affect the shape of these ion channels.
Ion channels that change their structure in response to voltage changes are called voltage-gated ion channels.

The ion channels regulate the concentrations of the different cations inside and outside the cell.

The ion channels are voltage-gated.

They will not open in response to a signal for a short time after activation.

The basis of the resting potential is discussed in this video.

The inside of a cell is 70 mV more negative than the outside, and this number varies by neuron type and by species.

The resting membrane potential is caused by differences in the concentrations of ion inside and outside the cell.
The system would reach equilibrium if each type of ion flowed across the membrane.
There are different concentrations of ion inside and outside the cell, as shown by the difference in the number of positively charged K+) inside and outside the cell.
When the cell is not in use, K+ ion accumulate inside the cell due to a net movement.
Increasing the concentration of cations outside the cell and inside the cell creates a negative resting membrane potential.
The negative charge within the cell can be created by the cell being more impermeable to the ion movement than it is to the sodium ion movement.
At high concentrations within the cell, potassium and sodium ion are maintained, while at high concentrations outside of the cell, they are not.
The cell has channels that allow the two cations to diffuse.
The neurons have more channels for potassium and sodium.

The rate at which potassium diffuses out of the cell is much faster than the rate at which sodium leaks in.

The inside of the cell is negatively charged because more cations are leaving the cell than are entering.
The resting potential is maintained by the actions of the pump.
The inside of the cell is negatively charged when more cations are expelled than taken in.
chloride ion accumulate outside of the cell because they are repelled by negatively charged proteins in the cytoplasm

There are different concentrations inside and outside of the cell.

There are different concentrations of Na+ and K+ ion inside and outside the cell.

A nerve impulse causes Na+ to enter the cell.
K+ channels open and the cell becomes hyperpolarized at the peak action potential.

If the input is strong enough, a neuron can send the signal to the downstream neurons.

A chemical called a neurotransmitter is used in the transmission of a signal.

ion channels open when neurotransmitters bind to the dendrites.

The target neuron is depolarized by a sensory cell or another neuron.
Positive ion can enter the cell through the Na+ channels in the axon hillock.
The neuron is completely depolarized when the sodium channels open.
Once the threshold potential is reached, action potentials are considered an "all or nothing" event.
Once depolarization is complete, the cell needs to be set back to its resting potential.
The Na+ channels can't be opened.
K+ can leave the cell at the same time as voltage-gated K+ channels open.
As K+ ion leave the cell, the potential becomes negative.
At this point, the sodium channels will return to their resting state, meaning they are ready to open again if the potential again exceeds the threshold.
The extra K+ ion diffuses out of the cell through the potassium leakage channels, bringing the cell back to its resting potential.

The formation of an action potential can be divided into five steps.

The hyperpolarized membrane is not able to fire.

Amiodarone and procainamide, which are used to treat abnormal electrical activity in the heart, impede the movement of K+ through voltage-gated K+ channels.

The action potential is done down the axon when the axon is repolarized.

An overview of action potential is presented in a video.

To communicate information to another neuron, it must travel along the axon and reach the axon terminals.

The diameter of the axon and the axon's resistance to current leak affect the speed of action potential along an axon.
The axon is an axon that myelin acts as an axon that prevents current from leaving the axon.
Current leaks from previously insulated axon areas slow action potential conduction in demyelinating diseases.
These unmyelinated spaces are small and contain Na+ and K+ channels.
The action potential along the axon can be regenerated by the flow of ionized water through these channels.
The action potential would have to be continuously regenerated at every point along the axon since Na+ and K+ channels wouldn't be able to regenerate at specific points.
The channels only need to be present at the nodes and not along the entire axon to save energy.

There are gaps in myelin along axons.

The K+ and Na+ channels are voltage-gated.
There are action potentials that travel down the axon.

The "gap" is where information is sent from one neuron to another.

It's not universally true that the axon terminals and dendritic spines are the same.
There are dendrite-to-dendrite and axon-to-cell body synapses.
The presynaptic neuron is the one that sends the signal, and the postsynaptic neuron is the one that receives it.
Most of the neurons are presynaptic and postsynaptic.
There are two types of connections.

When an action potential reaches the axon terminal it opens the Na+ channels.

Ca2+ channels open because of this depolarization.

The image is from a scanning electron microscope.

This pseudocolored image was taken with a scanning electron microscope and shows an axon terminal that was broken open.

The neurotransmitter diffuses across the synaptic cleft.

Communication at chemical synapses requires the release of neurotransmitters.

Ca2+ can enter the cell when the presynaptic membrane is depolarized.
The calcium entry causes the synaptic cleft to open.
A depolarization or hyperpolarization of the postsynaptic neuron can occur when the neurotransmitter diffuses across the synaptic cleft.

The binding of a specific neurotransmitter causes certain ion channels to open.

Table 35.1 shows the excitatory and inhibitory effects of transmitters.
When acetylcholine is released by a presynaptic neuron, it causes postsynaptic Na+ channels to open.
Na+ enters the postsynaptic cell.
When the neurotransmitter GABA is released from a presynaptic neuron, it can bind to and open the Cl- channels.
The neuron is less likely to fire an action potential if the cell is hyperpolarized.

The neurotransmitter must be removed from the synaptic cleft in order for the postsynaptic membrane to be ready to receive another signal.

The neurotransmitter can diffuse away from the synaptic cleft, it can be degraded by the synaptic cleft, or it can be recycled by the presynaptic neuron.
Some drugs that are given to Alzheimer's patients work by blocking the acetylcholinesterase.
The increase in acetylcholine release is caused by the inhibition of the enzyme.
Once released, the chyln stays in the cleft and can bind and unbind postsynaptic receptors.

The electrical and chemical sphinxes are found in all nervous systems and play important and unique roles.

The mode of transmission in electrical and chemical synapses is different.
The presynaptic and postsynaptic membranes are very close together and are physically connected.
Current can be passed directly from one cell to the next.
In addition to the ion that carries the current, other molecule can diffuse through the large gap junction pores.

There are differences between chemical and electrical connections.

There is a one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter opens the postsynaptic ion channels.
This signaling is not one-way.
In contrast, signaling in electrical synapses is almost instantaneous, and some electrical synapses are not.

As they are less likely to be blocked, electrical synapses are more reliable, and they are important for synchronizing the electrical activity of a group of neurons.

Slow-wave sleep is thought to be regulated by electrical synapses in the thalamus.

Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron, but often multiple presynaptic inputs must create them around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential.

One neuron often has inputs from many presynaptic neurons, so IPSPs can cancel out EPSPs and vice versa.
It is the net change in the postsynaptic voltage that determines if the postsynaptic cell has reached its threshold.
Random "noise" in the system is not transmitted as important information if the threshold for excitation and synaptic summation are combined.

A single neuron can receive both excitatory and inhibitory inputs.

At the axon hillock, all these inputs are added together.
The neuron will fire if the EPSPs are strong enough to overcome the IPSPs.

Lou Gehrig's Disease is a neurological disease characterized by the loss of motor neurons that control voluntary movements.

In the end, the disease can lead to paralysis due to the destruction of the neurons that control speech, breathing, and swallowing.
Patients need assistance from machines to breathe and communicate.

"locked-in" patients can communicate with the rest of the world using special technologies.

One technology allows patients to type out sentences by twitching their cheek.

The sentences can be read by a computer.

Brain-Computer interface (BCI) technology is a relatively new line of research for helping paralyzed patients communicate and retain a degree of self-sufficiency.

There are different forms of BCI.
Some forms use electrical stimulation on the skull.
The recordings contain information that can be deciphered by a computer.
This form of BCI is more powerful than the other forms as each electrode can record action potentials from one or more neurons.
The signals are sent to a computer, which is trained to decode them and send them to a tool.
Even though the paralyzed patient cannot move his or her hand or arm, he or she can use e-mail, read the Internet, and communicate with others by thinking of moving his or her hand or arm.
A paralyzedlocked-in patient who suffered a stroke 15 years ago has been able to control a robotic arm and even eat coffee using BCI technology.

BCI technology is amazing, but it also has limitations.

The technology can require many hours of training and long periods of intense concentration for the patient, as well as brain surgery to implant the devices.

Neural signals from a paralyzed patient are collected, decoded, and fed to a tool, such as a computer, a wheelchair, or a robotic arm.

In this video, a paralyzed woman uses a brain-controlled robotic arm to bring a drink to her mouth, among other images of brain- computer interface technology in action.

Synapses are not static structures.

New synapses can be made if they are broken.

These changes are needed for a functioning nervous system.

The basis of learning and memory is synaptic plasticity.
Long-term potentiation and long-term depression are important forms of synaptic plasticity that occur in the hippocampus, a brain region that is involved in storing memories.

The Hebbian principle states that cells that fire together wire together.

There are many mechanisms behind the synaptic strength seen with LTP.
When the postsynaptic neuron is depolarized by multiple presynaptic inputs in quick succession, the magnesium ion are forced out, allowing Ca ion to pass into the postsynaptic cell.
Next, Ca2+ ion entering the cell causes a signaling cascade that causes a different type of glutamate receptor to be inserted into the postsynaptic membrane.
When glutamate is released from the presynaptic membrane, it will cause a larger excitatory effect on the postsynaptic cell because it will allow more positive ion into the cell.
The postsynaptic neuron is more likely to fire in response to presynaptic neurotransmitter release if there is additional AMPA receptors.
Drug abuse can lead to addiction by co-opting the LTP pathway.